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1
Trifunović, Svetlana, Branka Šošić Jurjević, Nataša Ristić, et al. "Maternal Dexamethasone Exposure Induces Sex-Specific Changes in Histomorphology and Redox Homeostasis of Rat Placenta." International Journal of Molecular Sciences 24, no. 1 (2022): 540. http://dx.doi.org/10.3390/ijms24010540.
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As the mediator between the mother and fetus, the placenta allows the most appropriate environment and optimal fetal growth. The placenta of one sex sometimes has a greater ability over the other to respond to and protect against possible maternal insults. Here, we characterized sex differences in the placenta’s morphological features and antioxidant status following dexamethasone (Dx) exposure. Pregnant rats were exposed to Dx or saline. The placenta was histologically and stereologically analyzed. The activity of the antioxidant enzymes, lipid peroxides (TBARS), superoxide anion and nitric oxide (NO) was measured. The decrease in placental zone volumes was more pronounced (p < 0.05) in female placentas. The volume density of PCNA-immunopositive nuclei was reduced (p < 0.05) in both sexes. The reduced (p < 0.05) antioxidant enzyme activities, enhanced TBARS and NO concentration indicate that Dx exposure triggered oxidative stress in the placenta of both fetal sexes, albeit stronger in the placenta of female fetuses. In conclusion, maternal Dx treatment reduced the size and volume of placental zones, altered placental histomorphology, decreased cell proliferation and triggered oxidative stress; however, the placentas of female fetuses exerted more significant responses to the treatment effects. The reduced placental size most probably reduced the transport of nutrients and oxygen, thus resulting in the reduced weight of fetuses, similar in both sexes. The lesser ability of the male placenta to detect and react to maternal exposure to environmental challenges may lead to long-standing health effects.
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Achur, Rajeshwara N., Sean T. Agbor-Enoh, and D. Channe Gowda. "Rat Spongiotrophoblast-specific Protein Is Predominantly a Unique Low Sulfated Chondroitin Sulfate Proteoglycan." Journal of Biological Chemistry 281, no. 43 (2006): 32327–34. http://dx.doi.org/10.1074/jbc.m605841200.
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We have previously demonstrated that the human placenta contains a uniquely low sulfated extracellular aggrecan family chondroitin sulfate proteoglycan (CSPG). This CSPG is a major receptor for the adherence of Plasmodium falciparum-infected red blood cells (IRBCs) in placentas, causing pregnancy-specific malaria. However, it is not known whether such low sulfated CSPGs occur in placentas of other animals and, if so, whether IRBCs bind to those CSPGs. In this study, we show that rat placenta contains a uniquely low sulfated extracellular CSPG bearing chondroitin sulfate (CS) chains, which comprise only ∼2% 4-sulfated and the remainder nonsulfated disaccharides. Surprisingly, the core protein of the rat placental CSPG, unlike that of the human placental CSPG, is a spongiotrophoblast-specific protein (SSP), which is expressed in a pregnancy stage-dependent manner. The majority of rat placental SSP is present in the CSPG form, and only ∼10% occurs without CS chain substitution. Of the total SSP-CSPG in rat placenta, ∼57% is modified with a single CS chain, and ∼43% carries two CS chains. These data together with the previous finding on human placental CSPG suggest that the expression of low sulfated CSPG is a common feature of animal placentas. Our data also show that the unique species-specific difference in the biology of the rat and human placentas is reflected in the occurrence of completely different CSPG core protein types. Furthermore, the rat SSP-CSPG binds P. falciparum IRBCs in a CS chain-dependent manner. Since IRBCs have been reported to accumulate in the placentas of malaria parasite-infected rodents, our results have important implications for exploiting pregnant rats as a model for studying chondroitin 4-sulfate-based therapeutics for human placental malaria.
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Clifton, Vicki L., Phillip C. Owens, Phillip J. Robinson, and Roger Smith. "Identification and characterization of a corticotrophin-releasing hormone receptor in human placenta." European Journal of Endocrinology 133, no. 5 (1995): 591–97. http://dx.doi.org/10.1530/eje.0.1330591.
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Clifton VL, Owens PC, Robinson PJ, Smith R. Identification and characterization of a corticotrophinreleasing hormone receptor in human placenta. Eur J Endocrinol 1995;133:591–7. ISSN 0804–4643 Corticotrophin-releasing hormone (CRH) causes vasodilatation in the human fetal–placental circulation and has paracrine actions in placental tissue, suggesting that CRH receptors may be present in the human placenta. We have now identified and characterized placental CRH binding sites and compared them to those described previously in human myometrium and rat pituitary. Radiolabelled ovine CRH binding to placental membranes was pH-, time-, temperature- and divalent cation-dependent and was reversible in the presence of 1 μmol/l unlabelled ovine CRH. Scatchard analysis of placentae delivered vaginally or by elective caesarean section revealed dissociation constants (Kd) of 214.5 ± 84 pmol/l (N = 8) and 45.4 ± 23.9 pmol/l (N = 9), respectively. The Kd for caesarean placental binding sites was similar to that of human myometrium (59.6 pmol/l, N = 3) and rat pituitary (82.5 pmol/l, N = 3) receptors. However, in vaginally delivered placentae the CRH binding sites had a much lower affinity (p < 0.05). The receptor densities (Bmax) of vaginally delivered and caesarean-delivered placentae were 28.6 ± 9.6 and 6.1 ± 2.8 fmol/mg, respectively (p < 0.05). Chemical cross-linking studies using disuccinimidyl suberate indicated that the molecular weight of the CRH receptor in the placenta and rat pituitary is 75 kD. We conclude that there is a high-affinity population of CRH binding sites in the human placenta that are physicochemically similar to pituitary and myometrial CRH receptors. The CRH receptor properties in the placenta change in response to labour, when CRH levels in maternal blood are highest, suggesting that placental CRH may regulate its receptor. R Smith, Endocrinology Unit, John Hunter Hospital, Locked Bag 1, Hunter Regional Mail Centre, Newcastle, NSW 2310, Australia
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Charest, Phanie L., Vanessa Vrolyk, Pauline Herst, et al. "Histomorphologic Analysis of the Late-term Rat Fetus and Placenta." Toxicologic Pathology 46, no. 2 (2018): 158–68. http://dx.doi.org/10.1177/0192623318755135.
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Histological examination of the rat placenta and fetus is uncommon. Toxicological studies mainly rely on gross examination of the fetus and on fetal and placental weights. These are often insufficient to assess the fetal and placental toxicity of xenobiotics. The small size of the fetus makes its dissection labor-intensive. Thus, our objective was to develop a simple and accurate technique to evaluate the rat fetus and placenta. Sprague-Dawley rat fetuses at gestational day 19.5 ( n = 18) and their placentas ( n = 32) were fixed in formalin. Placentas were cut transversally in the center. Fetuses were cut following a freehand whole-body serial sectioning diagram adapted from Wilson’s method. Sections were stained with hematoxylin–eosin–phloxine–saffron, and histomorphometry was used to measure the area of the fetal placental region (27.2 ± 1.7 mm2), including the labyrinth (22.2 ± 1.0 mm2) and the basal zone (4.8 ± 0.8 mm2). Our whole-fetus serial sectioning technique resulted in 12 precise cutting planes that fit on 3 histological slides, enabling the examination of most organs without labor-intensive dissection. Quantitative analysis of placental areas improves the understanding of the pathogenesis of treatment-related changes. This technique provides a standardized method for future research in pertinent fields such as developmental biology and toxicology.
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Borke, James L., Ariel Caride, Anil K. Verma, et al. "Calcium pump epitopes in placental trophoblast basal plasma membranes." American Journal of Physiology-Cell Physiology 257, no. 2 (1989): C341—C346. http://dx.doi.org/10.1152/ajpcell.1989.257.2.c341.
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The syncytiotrophoblast represents the primary cellular barrier between maternal and fetal circulations in the placenta. Large amounts of Ca2+ are transported across this barrier by mechanisms that are not clearly understood. To further understand this phenomenon, we examined rat and human placenta by immunohistochemical and protein blotting techniques with a monoclonal antibody raised against the human erythrocyte plasma membrane Ca2+ pump. Immunohistochemistry with this antibody showed specific staining in the human placenta of the basal (fetal facing) surface of the syncytiotrophoblast. In the rat placenta, immunohistochemistry also showed specific staining of the innermost (fetal facing) layer of the trophoblast and the basal surface of the endoderm of the intraplacental yolk sac. In Western blots of placental homogenates and membranes, the monoclonal antibody bound to a 140,000-mol wt band, characteristic of Ca2+ pumps in other tissues. Western blots of isolated basal membranes showed more intense staining than isolated microvillous membranes, confirming the results of the immunohistochemistry. In addition, Ca2+ transport in basal membrane vesicles from human placenta was inhibited by polyclonal antibodies prepared against the erythrocyte Ca2+ pump. We conclude that basal (fetal facing) layers of human and rat placentas contain a high-affinity Ca2+ pump situated to transport Ca2+ from the maternal to the fetal circulation. calcium-magnesium-adenosinetriphosphatase; calcium transport; immunohistochemistry; rat and human placenta Submitted on November 14, 1988 Accepted on March 27, 1989
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Lacroix, MC, H. Jammes, and G. Kann. "Occurrence of a growth hormone-releasing hormone-like messenger ribonucleic acid and immunoreactive peptide in the sheep placenta." Reproduction, Fertility and Development 8, no. 3 (1996): 449. http://dx.doi.org/10.1071/rd9960449.
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Growth hormone releasing factor (GHRH) has been described in the rat, mouse and human placentae. This study reports the presence of an immunoreactive GHRH activity (IR-GHRH) in the ovine placenta. This activity was detected by radioimmunoassay from day 50 (D50) until the end of pregnancy. Higher IR-GHRH concentration in placental tissue was observed on days 100 (543 +/- 123 pg/g) and 140 (550 +/- 62 pg/g) and, when compared with the GHRH content of the ovine hypothalamus (1.2 ng/hypothalamus), represents a considerable amount of GHRH per placenta (a mean of 200 ng). Perifused placenta explants released IR-GHRH in vitro at a mean rate of 200 pg/g/h. Depolarization by 55 mM KCl increased the IR-GHRH concentration of the perifusion media 1.7 times over basal values. The elution position of GHRH immunoreactivity in the gel filtration chromatography profiles was the same for placenta and hypothalamus extracts and lay very near to the molecular weight of bovine GHRH. Northern blot hybridization analysis revealed the existence of a placental transcript whose size (0.75 kb) was comparable to the size of the ovine hypothalamus and rat placenta GHRH transcripts. Hybridization signal was observed at each stage studied from D50 until D120 of pregnancy. This study demonstrated the existence of a IR-GHRH peptide in the ovine placenta.
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Shearman, Lauren P., Alison M. McReynolds, Feng C. Zhou, and Jerrold S. Meyer. "Relationship between [125I]RTI-55-labeled cocaine binding sites and the serotonin transporter in rat placenta." American Journal of Physiology-Cell Physiology 275, no. 6 (1998): C1621—C1629. http://dx.doi.org/10.1152/ajpcell.1998.275.6.c1621.
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We investigated the characteristics of cocainelike binding sites in rat placenta using [125I]RTI-55. [3H]paroxetine binding and immunocytochemical staining for serotonin [5-hydroxytryptamine (5-HT)] and for the 5-HT transporter were also used to obtain evidence for rat placental 5-HT uptake. [125I]RTI-55 saturation analyses with membranes from normal gestational day 20 placentas yielded curvilinear Scatchard plots that were resolved into high- and low-affinity components (mean dissociation constants of 0.29 and 7.9 nM, respectively). Drug competition studies with various monoamine uptake inhibitors gave rise to complex multiphasic displacement curves, although the results obtained with the selective 5-HT uptake inhibitor citalopram suggest that the 5-HT transporter is an important component of placental high-affinity [125I]RTI-55 binding. The presence of a rat placental 5-HT uptake system was additionally supported by the [3H]paroxetine binding experiments and by the presence throughout the placenta of immunoreactivity for 5-HT and the 5-HT transporter. Immunostaining with both antibodies was most intense in the junctional zone, whereas the density of [125I]RTI-55 binding sites was greater in the placental labyrinth. This discrepancy may be due to the fact that [125I]RTI-55 appears to be labeling additional cellular components besides the 5-HT transporter. The presence of cocaine- and antidepressant-sensitive 5-HT transporters in the placenta has important implications for the possible effects of these compounds on pregnancy and fetal development.
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White, Elizabeth A., Joffre B. Baker, Michael McGrogan, and Paul A. Kitos. "Protease Nexin 1 Is Expressed in the Human Placenta." Thrombosis and Haemostasis 69, no. 02 (1993): 119–23. http://dx.doi.org/10.1055/s-0038-1651566.
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SummaryProtease nexin 1 (PN1), a serine protease inhibitor that inactivates thrombin, urokinase, and plasmin, is produced abundantly in cultures of human fibroblasts and rat and human glioma cells. The major sites of PN1 synthesis in vivo and the specific physiological function(s) of this serpin are unknown. Using Northern blot analysis and a full-length PN1 cDNA probe we demonstrated the presence of PN1 mRNA in human term placentas. In situ hybridization of placental tissue with a PN1 riboprobe showed that PN1 mRNA is present throughout the placenta and is also abundant in the placental membranes. Immunohistochemical analysis with an anti-PN1 antibody showed co-localization of PN1 and its mRNA within the placenta.
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Vaswani, Kanchan, Hsiu-Wen Chan, Hassendrini N. Peiris, et al. "Gestation Related Gene Expression of the Endocannabinoid Pathway in Rat Placenta." Mediators of Inflammation 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/850471.
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Mammalian placentation is a vital facet of the development of a healthy and viable offspring. Throughout gestation the placenta changes to accommodate, provide for, and meet the demands of a growing fetus. Gestational gene expression is a crucial part of placenta development. The endocannabinoid pathway is activated in the placenta and decidual tissues throughout pregnancy and aberrant endocannabinoid signaling during the period of placental development has been associated with pregnancy disorders. In this study, the gene expression of eight endocannabinoid system enzymes was investigated throughout gestation. Rat placentae were obtained at E14.25, E15.25, E17.25, and E20, RNA was extracted, and microarray was performed. Gene expression of enzymesFaah, Mgll, Plcd4, Pld1, Nat1, Daglα, andPtgs2was studied (cohort 1, microarray). Biological replication of the results was performed by qPCR (cohort 2). Four genes showed differential expression (Mgll, Plcd4, Ptgs2, and Pld1), from mid to late gestation. Genes positively associated with gestational age werePtgs2, Mgll, and Pld1, whilePlcd4was downregulated. This is the first comprehensive study that has investigated endocannabinoid pathway gene expression during rat pregnancy. This study provides the framework for future studies that investigate the role of endocannabinoid system during pregnancy.
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Sobočan, Nikola, Marta Himelreich-Perić, Ana Katušić-Bojanac та ін. "Extended Prophylactic Effect of N-tert-Butyl-α-phenylnitron against Oxidative/Nitrosative Damage Caused by the DNA-Hypomethylating Drug 5-Azacytidine in the Rat Placenta". International Journal of Molecular Sciences 23, № 2 (2022): 603. http://dx.doi.org/10.3390/ijms23020603.
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Antioxidant N-tert-Butyl-α-phenylnitron (PBN) partly protected embryos from the negative effects of a DNA demethylating drug 5-azacytidine during pregnancy. Our aim was to investigate PBN’s impact on the placenta. Fischer rat dams were treated on gestation days (GD) 12 and 13 by PBN (40 mg/kg), followed by 5azaC (5 mg/kg) after one hour. Global methylation was assessed by pyrosequencing. Numerical density was calculated from immunohistochemical expression in single cells for proliferating (PCNA), oxidative (oxoguanosine) and nitrosative (nitrotyrosine) activity. Results were compared with the PBN-treated and control rats. PBN-pretreatment significantly increased placental weight at GD15 and GD20, diminished by 5azaC, and diminished apoptosis in GD 20 placentas caused by 5azaC. Oxoguanosine expression in placentas of 5azaC-treated dams was especially high in the placental labyrinth on GD 15, while PBN-pretreatment lowered its expression on GD 15 and GD 20 in both the labyrinth and basal layer. 5azaC enhanced nitrotyrosine level in the labyrinth of both gestational stages, while PBN-pretreatment lowered it. We conclude that PBN exerted its prophylactic activity against DNA hypomethylating agent 5azaC in the placenta through free radical scavenging, especially in the labyrinthine part of the placenta until the last day of pregnancy.
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Reyes-Hernández, Cynthia, David Ramiro-Cortijo, Pilar Rodríguez-Rodríguez, et al. "Effects of Arachidonic and Docosohexahenoic Acid Supplementation during Gestation in Rats. Implication of Placental Oxidative Stress." International Journal of Molecular Sciences 19, no. 12 (2018): 3863. http://dx.doi.org/10.3390/ijms19123863.
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Arachidonic and docosahexaenoic acids (ARA and DHA) are important during pregnancy. However, the effects of dietary supplementation on fetal growth and oxidative stress are inconclusive. We aimed to assess the effect of high ARA and DHA diet during rat gestation on: (1) ARA and DHA availability in plasma and placenta, (2) fetal growth, and (3) placental oxidative stress, analyzing the influence of sex. Experimental diet (ED) was prepared by substituting soybean oil in the control diet (CD) by a fungi/algae-based oil containing ARA and DHA (2:1). Rats were fed with CD or ED during gestation; plasma, placenta, and fetuses were obtained at gestational day 20. DHA, ARA, and their precursors were analyzed in maternal plasma and placenta by gas chromatography/mass spectrophotometry. Fetuses and placentas were weighed, the proportion of fetuses with intrauterine growth restriction (IUGR) determined, and placental lipid and protein oxidation analyzed. ED fetuses exhibited lower body weight compared to CD, being >40% IUGR; fetal weight negatively correlated with maternal plasma ARA, but not DHA. Only ED female placenta exhibited higher lipid and protein oxidation compared to its CD counterparts; lipid peroxidation is negatively associated with fetal weight. In conclusion, high ARA during gestation associates with IUGR, through placental oxidative stress, with females being more susceptible.
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Shaw, A. J., M. Z. Mughal, M. J. Maresh, and C. P. Sibley. "Sodium-dependent magnesium transport across in situ perfused rat placenta." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 2 (1991): R369—R372. http://dx.doi.org/10.1152/ajpregu.1991.261.2.r369.
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Placentas of anesthetized rats were perfused in situ on the fetal side to study mechanisms of Mg2+ transport. The perfusate was a Mg(2+)-free Krebs-Ringer, and the unidirectional transfer of Mg2+ from maternal plasma to this Ringer was compared with that of 45Ca and 51Cr-EDTA, the latter being employed as a paracellular diffusional marker. Placental perfusion with amiloride (0.5 mM) or ouabain (1 mM) both rapidly (4 min) reduced maternal-fetal clearance (Kmf) for Mg2+ but had no effect on Kmf for 45Ca. In contrast, perfusion of the carbonic anhydrase inhibitor acetazolamide (1 mM) did not affect Kmf for Mg2+ or 45Ca. Placental perfusion with a Na+-free Ringer reduced Kmf for both Mg2+ and 45Ca, although the latter response was delayed. Kmf for 51Cr-EDTA was increased by amiloride and was unaffected by perfusion of ouabain, acetazolamide, or Na+-free Ringer, indicating that the effects of these treatments on Kmf of Mg2+ do not reflect nonspecific effects on placental permeability. These data suggest that maternal-fetal transfer of Mg2+ across the perfused rat placenta is Na+ dependent.
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Sawa, Hiroki, Hiroyuki Ukita, Minoru Fukuda, Hajime Kamada, Isamu Saito, and Björn öbrink. "Spatiotemporal Expression of C-CAM in the Rat Placenta." Journal of Histochemistry & Cytochemistry 45, no. 7 (1997): 1021–34. http://dx.doi.org/10.1177/002215549704500711.
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We investigated the expression of the immunoglobulin superfamily cell adhesion molecule, C-CAM, in developing and mature rat placenta. By immunohistochemical staining at the light microscopic level, no C-CAM-expression was seen before Day 9 of gestation, when it appeared in the trophoblasts of ectoplacental cones. On Day 10.5, spongiotrophoblasts and invasive trophoblasts around the maternal vessels of the decidua basalis were stained positively. On Day 12.5, C-CAM was detected in the spongiotrophoblasts of the junctional layer, but labyrinth trophoblasts and secondary giant trophoblasts were not stained. On Day 17.5, C-CAM was found only in the labyrinth and lacunae of the junctional layer. At this stage, both the labyrinth cytotrophoblasts of the maternal blood vessels and the endothelial cells of the embryonic capillaries were strongly stained. Placental tissues from gestational Days 12.5 and 17.5 were analyzed by immunoelectron microscopy to determine the location of C-CAM at the subcellular level. On Day 12.5, positive staining of the spongiotrophoblasts was observed, mainly on surface membranes and microvilli between loosely associated cells. On Day 17.5, staining was found primarily on the microvilli of the maternal luminal surfaces of the labyrinth cytotrophoblasts, and both on the luminal surface and in the cytoplasm of endothelial cells of the embryonic vessels. RT-PCR analysis and Southern blotting of the PCR products revealed expression of mRNA species for both of the major isoforms, C-CAM1 and C-CAM2. Immunoblotting analysis of C-CAM isolated from 12.5-day and 14.5-day placentae showed that it appeared as a broad band with an apparent molecular mass of 110–170 kD. In summary, C-CAM was strongly expressed in a specific spatiotemporal pattern in trophoblasts actively involved in formation of the placental tissue, suggesting an important role in placental development. In the mature placenta, C-CAM expression was confined to the trophoblastic and endothelial cells lining the maternal and embryonic vessels, respectively, suggesting important functions in placental physiology.
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Cho, Jae-Hyeon, Hiromichi Kimura, Tatsuya Minami, et al. "DNA Methylation Regulates Placental Lactogen I Gene Expression." Endocrinology 142, no. 8 (2001): 3389–96. http://dx.doi.org/10.1210/endo.142.8.8347.
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Abstract Expression of rat placental lactogen I is specific to the placenta and never expressed in other tissues. To obtain insight into the mechanism of tissue-specific gene expression, we investigated the methylation status in 3.4 kb of the 5′-flanking region of the rat placental lactogen I gene. We found that the distal promoter region of the rat placental lactogen I gene had more potent promoter activity than that of the proximal area alone, which contains several possible cis-elements. Although there are only 17 CpGs in the promoter region, in vitro methylation of the reporter constructs caused severe suppression of reporter activity, and CpG sites in the placenta were more hypomethylated than other tissues. Coexpression of methyl-CpG-binding protein with reporter constructs elicited further suppression of the reporter activity, whereas treatment with trichostatin A, an inhibitor of histone deacetylase, reversed the suppression caused by methylation. Furthermore, treatment of rat placental lactogen I nonexpressing BRL cells with 5-aza-2′-deoxycytidine, an inhibitor of DNA methylation, or trichostatin A resulted in the de novo expression of rat placental lactogen I. These results provide evidence that change in DNA methylation is the fundamental mechanism regulating the tissue-specific expression of the rat placental lactogen I gene.
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Berghorn, K. A., P. A. Clark, B. Encarnacion, et al. "Developmental expression of the homeobox protein Distal-less 3 and its relationship to progesterone production in mouse placenta." Journal of Endocrinology 186, no. 2 (2005): 315–23. http://dx.doi.org/10.1677/joe.1.06217.
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Distal-less 3 (Dlx3) is a homeobox factor that functions as a placental-specific transcriptional regulator. Dlx3 null mice (−/−) have compromised placental development and do not survive in utero past embryonic day (E) 9.5. The current studies were undertaken to examine the expression of Dlx3 in mouse placenta during gestation, and to determine whether Dlx3 was involved in placental progesterone production. Dlx3 was not detectable at E8.5 but was detected in E9.5 placenta with continuing but diminished expression through E15.5. Dlx3 immuno-localization was restricted to the labyrinth, was nuclear and was found in cytokeratin-positive cells. Previous studies in choriocarcinoma cell lines support the conclusion that Dlx3 is required for expression of 3′-hydroxysteroid dehydrogenase VI (3βHSD VI), an obligate enzyme in the production of progesterone by trophoblast giant cells. In a rat trophoblast stem cell line (Rcho-1), Dlx3 expression was non-detectable in Rcho-1 cells induced to differ-entiate using mitogen withdrawal. In vitro progesterone production in placental cultures and 3βHSD VI mRNA from Dlx3 (+/+), (+/−) and (−/−) mice were equivalent. In situ hybridization for 3βHSD VI revealed mRNA expression restricted to trophoblast giants cells with no detectable expression in the labyrinth suggesting that Dlx3 and 3βHSD VI were not colocalized within the placenta. These studies support the conclusion that Dlx3 protein expression is restricted to the labyrinth region of the murine placenta into late gestation and that Dlx3 does not appear to be expressed in trophoblast giant cells. Further, loss of Dlx3 was not correlated with synthesis of progesterone from E9.5 mouse placentas.
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Jones, M. L., P. J. Mark, T. A. Mori, and B. J. Waddell. "523. PLACENTAL ANTIOXIDANT ENZYMES IN RAT PREGNANCY SHOW ZONE- AND STAGE-DEPENDENT VARIATION." Reproduction, Fertility and Development 21, no. 9 (2009): 122. http://dx.doi.org/10.1071/srb09abs523.
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Placental oxidative stress plays a key role in the pathophysiology of placenta-related disorders including preeclampsia. Protection from oxidative stress is provided by antioxidant enzymes which inactivate reactive oxygen species (ROS). The rat placenta consists of two major zones, the junctional (JZ) and labyrinth (LZ), and because only the LZ grows in late gestation we hypothesized it generates more ROS and thus requires greater antioxidant protection. Our previous studies on expression of the antioxidants superoxide dismutase (SOD)-1, SOD-2 and catalase support this hypothesis. Here, we extend these observations to include mRNA expression of SOD-3 and thioredoxin reductases (Txnrd-1, -2, -3) and activities of SOD, hydrogen peroxide (H2O2) scavenging and xanthine oxidase (XO). Placental oxidative damage was assessed by measurement of F2-isoprostanes and TBARS concentrations. We also measured the effects of maternal dexamethasone treatment, since glucocorticoid excess is known to induce oxidative damage in other tissues. Placentas were collected from untreated mothers on days 16 and 22 (term=day 23) and on day 22 after dexamethasone treatment from day 13 (1 μg/ml drinking water). SOD-3, Txnrd-1, -2, and -3 mRNAs were measured in JZ and LZ by qRT-PCR. F2-isoprostanes were measured by GC-MS and kit assays were used to measure TBARS and the activities of SOD, H2O2 scavenging and XO. In both placental zones, expression of SOD-3 and Txnrd-1 mRNAs and H2O2 scavenging activity decreased from day 16 to 22, whereas XO activity increased. Dexamethasone treatment increased H2O2 scavenging in both zones, but had no effect on SOD or XO activities or antioxidant mRNA expression. Despite predicted increases in placental ROS generation in late pregnancy and after dexamethasone, neither F2-isoprostanes nor TBARS were increased. These and our previous data suggest that endogenous protection against oxidative stress is abundant in the rat placenta and provides protection against potential oxidative insults including glucocorticoid excess.
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Purnama, Jeri Nobia, Erick Khristian, Mas Rizky A. A. Syamsunarno, Ramdan Panigoro, and Ratu Safitri. "The Effect of Sappan Wood Extract (Caesalpinia sappan L.) on Fetal and Placenta Histopathology of White Rat." Jurnal Veteriner 23, no. 2 (2022): 166–74. http://dx.doi.org/10.19087/jveteriner.2022.23.2.166.
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Histomorphological assessment of the placenta and fetus was more effective in assessing fetal development on a research scale for determined an active substance during the gestation period in experimental animals. The placenta and fetus connect in the development process. This study aimed to analyze the effect of giving ethanol extract of sappanwood on white rats’ placenta and fetal organs, which were examined histologically at 20 days pregnant rats. The pregnant rats were divided into six groups: The negative group was given aquadest, and treatment groups were given an ethanolic Sappan wood extract 100;200;300;400;500 mg/kg BW. Euthanized with CO2 and cesarian section was performed on pregnant rats on the 20th gestational day. Observation to record fetal body weight, body length, mean placental weight, and the histology of the placental area. Histomorphometry was used to measure the area of the fetal placental region. The group with sappan wood extract had no statistically significant difference in fetal body weight, fetal body length, fetal tail length, the weight placenta, and histomorphometry of the placenta compared to the control group (p > 0.05); this showed that the ethanolic extract of sappan wood does not have a toxic effect on the development of the placenta, which can interfere with fetal development during pregnancy. Sappan wood extract had a nontoxic effect on the placenta and fetal rat development on histological examination, even at the highest dose of 500 mg.kg-1 bw.
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Sahgal, N., GT Knipp, B. Liu, BM Chapman, G. Dai, and MJ Soares. "Identification of two new nonclassical members of the rat prolactin family." Journal of Molecular Endocrinology 24, no. 1 (2000): 95–108. http://dx.doi.org/10.1677/jme.0.0240095.
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The prolactin (PRL) family is comprised of a group of hormones/cytokines that are expressed in the anterior pituitary, uterus, and placenta. These proteins participate in the control of maternal and fetal adaptations to pregnancy. In this report, we have identified two new nonclassical members of the rat PRL family through a search of the National Center for Biotechnology Information dbEST database. The cDNAs were sequenced and their corresponding mRNAs characterized. Overall, the rat cDNAs showed considerable structural similarities with mouse proliferin-related protein (PLF-RP) and prolactin-like protein-F (PLP-F), consistent with their classification as rat homologs for PLF-RP and PLP-F. The expression of both cytokines/hormones was restricted to the placenta. The intraplacental sites of PLF-RP and PLP-F synthesis differed in the rat and the mouse. In the mouse, PLF-RP was expressed in the trophoblast giant cell layer of the midgestation chorioallantoic and choriovitelline placentas and, during later gestation, in the trophoblast giant cell and spongiotrophoblast layers within the junctional zone of the mouse chorioallantoic placenta. In contrast, in the rat, PLF-RP was first expressed in the primordium of the chorioallantoic placenta (ectoplacental cone region) and, later, exclusively within the labyrinth zone of the chorioallantoic placenta. In the mouse, PLP-F is an exclusive product of the spongiotrophoblast layer, whereas in the rat, trophoblast giant cells were found to be the major source of PLP-F, with a lesser contribution from spongiotrophoblast cells late in gestation. In summary, we have established the presence of PLF-RP and PLP-F in the rat.
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Draycott, Sally A. V., Zoe Daniel, Raheela Khan, Beverly S. Muhlhausler, Matthew J. Elmes, and Simon C. Langley-Evans. "Expression of cholesterol packaging and transport genes in human and rat placenta: impact of obesity and a high-fat diet." Journal of Developmental Origins of Health and Disease 11, no. 3 (2019): 222–27. http://dx.doi.org/10.1017/s2040174419000606.
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AbstractEvidence suggests that sub-optimal maternal nutrition has implications for the developing offspring. We have previously shown that exposure to a low-protein diet during gestation was associated with upregulation of genes associated with cholesterol transport and packaging within the placenta. This study aimed to elucidate the effect of altering maternal dietary linoleic acid (LA; omega-6) to alpha-linolenic acid (ALA; omega-6) ratios as well as total fat content on placental expression of genes associated with cholesterol transport. The potential for maternal body mass index (BMI) to be associated with expression of these genes in human placental samples was also evaluated. Placentas were collected from 24 Wistar rats at 20-day gestation (term = 21–22-day gestation) that had been fed one of four diets containing varying fatty acid compositions during pregnancy, and from 62 women at the time of delivery. Expression of 14 placental genes associated with cholesterol packaging and transfer was assessed in rodent and human samples by quantitative real time polymerase chain reaction. In rats, placental mRNA expression of ApoA2, ApoC2, Cubn, Fgg, Mttp and Ttr was significantly elevated (3–30 fold) in animals fed a high LA (36% fat) diet, suggesting increased cholesterol transport across the placenta in this group. In women, maternal BMI was associated with fewer inconsistent alterations in gene expression. In summary, sub-optimal maternal nutrition is associated with alterations in the expression of genes associated with cholesterol transport in a rat model. This may contribute to altered fetal development and potentially programme disease risk in later life. Further investigation of human placenta in response to specific dietary interventions is required.
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Wharfe, Michaela D., Peter J. Mark, and Brendan J. Waddell. "Circadian Variation in Placental and Hepatic Clock Genes in Rat Pregnancy." Endocrinology 152, no. 9 (2011): 3552–60. http://dx.doi.org/10.1210/en.2011-0081.
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Clock genes drive circadian rhythms in a range of physiological processes both centrally and in peripheral tissues such as the liver. The aims of this study were to determine whether the two functionally-distinct zones of the rat placenta (junctional and labyrinth) differentially express clock genes and, if so, whether these exhibit circadian patterns. Rats were sampled from d 21 of pregnancy (term = d 23) and from diestrus I of the estrous cycle. Adult liver (all animals), fetal liver, and placental zones (pregnant animals) were collected at 0800, 1400, 2000, and 0200 h. Both zones of the rat placenta expressed all seven canonical clock genes (Clock, Bmal1, Per1, Per2, Per3, Cry1, and Cry2), but there were marked zonal differences and, unlike in maternal liver, circadian variation in placenta was limited. Similarly, placental expression of Vegf varied with zone but not time of day. Pregnancy also led to marked changes in hepatic clock gene expression, with peak levels of Per1, Cry1, and Cry2 all reduced, Per3 increased, and circadian variation in Clock expression lost. All clock genes were expressed in fetal liver, but there was less circadian variation than in maternal liver. Similarly, fetal corticosterone levels remained stable across the day, whereas maternal corticosterone showed clear circadian variation. In conclusion, our data show that the rat placenta expresses all canonical clock genes in a highly zone-specific manner but with relatively little circadian variation. Moreover, pregnancy alters the expression and circadian variation of clock genes in maternal liver, possibly contributing to maternal physiological adaptations.
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Waddell, B. J. "056. EUTHERIAN MAMMALS DO IT DIFFERENTLY: PLACENTAL ENDOCRINE STRATEGIES FOR THE MAINTENANCE OF PREGNANCY IN RODENTS AND PRIMATES." Reproduction, Fertility and Development 22, no. 9 (2010): 17. http://dx.doi.org/10.1071/srb10abs056.
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The placenta of rats and humans share important anatomical similarities, each with a chorio-allantoic, single discoid, haemochorial structure that facilitates highly efficient nutrient transport. Importantly, however, these similarities reflect convergent evolution and conceal markedly different developmental trajectories and endocrine functions. Placental endocrine signals are essential to drive maternal adaptations that facilitate fetal development and ultimately successful birth. Central to these adaptations is a sustained increase in production of the sex steroids progesterone and oestrogen, each driven by very different placental signalling in rodents and primates. Specifically, while the rat placenta supplies androgen precursors for ovarian (luteal) oestrogen synthesis, in humans and closely-related primates the fetal adrenal cortex supplies androgen precursors for placental oestrogen synthesis. In both cases the resultant increase in oestrogen provides a local stimulus to ovarian (rat) and placental (primate) progesterone synthesis. This shift from a placental-ovarian to a feto-placental unit for oestrogen synthesis in primates may have evolved to ensure greater fetal influence over maternal adaptations. Placental regulation of maternal physiology is also mediated via a third steroid group, the glucocorticoids, which promote a successful pregnancy outcome via effects on maternal metabolism and fetal organ maturation. Glucocorticoids are produced within the HPA axis, activity of which is enhanced by the placenta (eg, via oestrogen in rodents and CRH in primates). Moreover, the placenta regulates access of maternal glucocorticoids to the fetus via expression of the 11 b -HSD enzymes which constitute the placental glucocorticoid barrier. Intriguingly, this barrier effectively disappears during late fetal life in rodents but increases markedly in primates (notably baboons and humans). We hypothesise that this opposite developmental change is due in part to the evolution of the feto-placental unit for oestrogen synthesis in these primate species, and the associated need to prevent suppression of the fetal HPA axis by maternal glucocorticoids in late gestation.
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Glazier, J. D., D. E. Atkinson, K. L. Thornburg, et al. "Gestational changes in Ca2+ transport across rat placenta and mRNA for calbindin9K and Ca(2+)-ATPase." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 4 (1992): R930—R935. http://dx.doi.org/10.1152/ajpregu.1992.263.4.r930.
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The unidirectional maternofetal clearance (Kmf) of 45Ca was measured across the rat placenta over the last one-third of gestation. Kmf for 45Ca normalized to its diffusion coefficient in water (Kmf/Dw) increased 72-fold between days 15 and 22 of gestation from 3.5 +/- 0.3 to 253.1 +/- 22.0 cm/g placenta, respectively. At 15 and 18 days of gestation, Kmf/Dw for 45Ca was similar to Kmf/Dw for the paracellular marker [14C]mannitol, but at 21 and 22 days of gestation, Kmf/Dw for 45Ca was significantly higher than Kmf/Dw for [14C]mannitol, indicating that an additional route of transfer, other than diffusion, becomes available to calcium during this period. Northern hybridization analysis demonstrated that rat placental calbindin9K-to-beta-actin mRNA ratio increased 135-fold between 15 and 22 days of gestation and was temporally associated with the gestational increase in Kmf/Dw for 45Ca. In contrast, rat placental Ca(2+)-ATPase-to-beta-actin mRNA ratio increased only two- to threefold over the same gestational period and did not mirror the gestational changes in calcium clearance. These trends suggest that the expression of placental calbindin9K, but not Ca(2+)-ATPase, may be rate limiting to placental calcium transport in the rat.
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Lovell, Tristan M., Russell J. Woods, David J. Butlin, et al. "Identification of a novel mammalian post-translational modification, phosphocholine, on placental secretory polypeptides." Journal of Molecular Endocrinology 39, no. 3 (2007): 189–98. http://dx.doi.org/10.1677/jme-07-0007.
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Placental neurokinin B appears to be post-translationally modified by phosphocholine (PC) attached to the aspartyl side chain at residue 4 of the mature peptide. Corticotrophin releasing factor (CRF) was found to be expressed by the rat placenta with the main secreted forms being phosphocholinated proCRF+/− one or two polysaccharide moieties. A combination of high-pressure liquid chromatography (HPLC) and two-site immunometric analysis suggested that PC was also attached to the placental precursors of adrenocorticotrophin, hemokinin, activin and follistatin. However, the fully processed forms of rat placental activin and CRF were free of PC. Formerly, the parasitic filarial nematodes have used PC as a post-translational modification, attached via the polysaccharide moiety of certain secretory glycoproteins to attenuate the host immune system allowing parasite survival, but it is the PC group itself which endows the carrier with the biological activity. The fact that treatment of proCRF peptides with phospholipase C but not endoglycosidase destroyed PC immunoreactivity suggested a simpler mode of attachment of PC to placental peptides than that used by nematodes. Thus, it is possible that by analogy the placenta uses its secreted phosphocholinated hormones to modulate the mother’s immune system and help protect the placenta from rejection.
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Mayeur, Sylvain, Steve Lancel, Nicolas Theys, et al. "Maternal calorie restriction modulates placental mitochondrial biogenesis and bioenergetic efficiency: putative involvement in fetoplacental growth defects in rats." American Journal of Physiology-Endocrinology and Metabolism 304, no. 1 (2013): E14—E22. http://dx.doi.org/10.1152/ajpendo.00332.2012.
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Low birth weight is associated with an increased risk for developing type 2 diabetes and metabolic diseases. The placental capacity to supply nutrients and oxygen to the fetus represents the main determiner of fetal growth. However, few studies have investigated the effects of maternal diet on the placenta. We explored placental adaptive proteomic processes implicated in response to maternal undernutrition. Rat term placentas from 70% food-restricted (FR30) mothers were used for a proteomic screen. Placental mitochondrial functions were evaluated using molecular and functional approaches, and ATP production was measured. FR30 drastically reduced placental and fetal weights. FR30 placentas displayed 14 proteins that were differentially expressed, including several mitochondrial proteins. FR30 induced a marked increase in placental mtDNA content and changes in mitochondrial functions, including modulation of the expression of genes implicated in biogenesis and bioenergetic pathways. FR30 mitochondria showed higher oxygen consumption but failed to maintain their ATP production. Maternal undernutrition induces placental mitochondrial abnormalities. Although an increase in biogenesis and bioenergetic efficiency was noted, placental ATP level was reduced. Our data suggest that placental mitochondrial defects may be implicated in fetoplacental pathologies.
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Horackova, Hana, Rona Karahoda, Lukas Cerveny, et al. "Effect of Selected Antidepressants on Placental Homeostasis of Serotonin: Maternal and Fetal Perspectives." Pharmaceutics 13, no. 8 (2021): 1306. http://dx.doi.org/10.3390/pharmaceutics13081306.
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Depression is a prevalent condition affecting up to 20% of pregnant women. Hence, more than 10% are prescribed antidepressant drugs, mainly serotonin reuptake inhibitors (SSRIs) and selective serotonin and noradrenaline reuptake inhibitors (SNRIs). We hypothesize that antidepressants disturb serotonin homeostasis in the fetoplacental unit by inhibiting serotonin transporter (SERT) and organic cation transporter 3 (OCT3) in the maternal- and fetal-facing placental membranes, respectively. Paroxetine, citalopram, fluoxetine, fluvoxamine, sertraline, and venlafaxine were tested in situ (rat term placenta perfusion) and ex vivo (uptake studies in membrane vesicles isolated from healthy human term placenta). All tested antidepressants significantly inhibited SERT- and OCT3-mediated serotonin uptake in a dose-dependent manner. Calculated half-maximal inhibitory concentrations (IC50) were in the range of therapeutic plasma concentrations. Using in vitro and in situ models, we further showed that the placental efflux transporters did not compromise mother-to-fetus transport of antidepressants. Collectively, we suggest that antidepressants have the potential to affect serotonin levels in the placenta or fetus when administered at therapeutic doses. Interestingly, the effect of antidepressants on serotonin homeostasis in rat placenta was sex dependent. As accurate fetal programming requires optimal serotonin levels in the fetoplacental unit throughout gestation, inhibition of SERT-/OCT3-mediated serotonin uptake may help explain the poor outcomes of antidepressant use in pregnancy.
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Rock, Kylie D., Brian Horman, Allison L. Phillips, et al. "EDC IMPACT: Molecular effects of developmental FM 550 exposure in Wistar rat placenta and fetal forebrain." Endocrine Connections 7, no. 2 (2018): 305–24. http://dx.doi.org/10.1530/ec-17-0373.
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Firemaster 550 (FM 550) is a flame retardant (FR) mixture that has become one of the most commonly used FRs in foam-based furniture and baby products. Human exposure to this commercial mixture, composed of brominated and organophosphate components, is widespread. We have repeatedly shown that developmental exposure can lead to sex-specific behavioral effects in rats. Accruing evidence of endocrine disruption and potential neurotoxicity has raised concerns regarding the neurodevelopmental effects of FM 550 exposure, but the specific mechanisms of action remains unclear. Additionally, we observed significant, and in some cases sex-specific, accumulation of FM 550 in placental tissue following gestational exposure. Because the placenta is an important source of hormones and neurotransmitters for the developing brain, it may be a critical target of toxicity to consider in the context of developmental neurotoxicity. Using a mixture of targeted and exploratory approaches, the goal of the present study was to identify possible mechanisms of action in the developing forebrain and placenta. Wistar rat dams were orally exposed to FM 550 (0, 300 or 1000 µg/day) for 10 days during gestation and placenta and fetal forebrain tissue collected for analysis. In placenta, evidence of endocrine, inflammatory and neurotransmitter signaling pathway disruption was identified. Notably, 5-HT turnover was reduced in placental tissue and fetal forebrains indicating that 5-HT signaling between the placenta and the embryonic brain may be disrupted. These findings demonstrate that environmental contaminants, like FM 550, have the potential to impact the developing brain by disrupting normal placental functions.
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Capobianco, E., A. Jawerbaum, M. C. Romanini та ін. "15-Deoxy-Δ12,14-prostaglandin J2 and peroxisome proliferator-activated receptor γ (PPARγ) levels in term placental tissues from control and diabetic rats: modulatory effects of a PPARγ agonist on nitridergic and lipid placental metabolism". Reproduction, Fertility and Development 17, № 4 (2005): 423. http://dx.doi.org/10.1071/rd04067.
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15-Deoxy-Δ12,14-prostaglandin J2 (15dPGJ2) is a peroxisome proliferator-activated receptor γ (PPARγ) ligand that regulates lipid homeostasis and has anti-inflammatory properties in many cell types. We postulated that 15dPGJ2 may regulate lipid homeostasis and nitric oxide (NO) levels in term placental tissues and that alterations in these pathways may be involved in diabetes-induced placental derangements. In the present study, we observed that, in term placental tissues from streptozotocin-induced diabetic rats, 15dPGJ2 concentrations were decreased (83%) and immunostaining for nitrotyrosine, indicating peroxynitrite-induced damage, was increased. In the presence of 15dPGJ2, concentrations of nitrates/nitrites (an index of NO production) were diminished (40%) in both control and diabetic rats, an effect that seems to be both dependent on and independent of PPARγ activation. Exogenous 15dPGJ2 did not modify lipid mass, but decreased the incorporation of 14C-acetate into triacylglycerol (35%), cholesteryl ester (55%) and phospholipid (32%) in placenta from control rats, an effect that appears to be dependent on PPARγ activation. In contrast, the addition of 15dPGJ2 did not alter de novo lipid synthesis in diabetic rat placenta, which showed decreased levels of PPARγ. We conclude that 15dPGJ2 modulates placental lipid metabolism and NO production. The concentration and function of 15dPGJ2 and concentrations of PPARγ were altered in placentas from diabetic rats, anomalies probably involved in diabetes-induced placental dysfunction.
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Lawrence, Dylan J., Kristie Huda, and Carolyn L. Bayer. "Longitudinal characterization of local perfusion of the rat placenta using contrast-enhanced ultrasound imaging." Interface Focus 9, no. 5 (2019): 20190024. http://dx.doi.org/10.1098/rsfs.2019.0024.
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The placenta performs many physiological functions critical for development. Insufficient placental perfusion, due to improper vascular remodelling, has been linked to many pregnancy-related diseases. To study longitudinal in vivo placental perfusion, we have implemented a pixel-wise time–intensity curve (TIC) analysis of contrast-enhanced ultrasound (CEUS) images. CEUS images were acquired of pregnant Sprague Dawley rats after bolus injections of gas-filled microbubble contrast agents. Conventionally, perfusion can be quantified using a TIC of contrast enhancement in an averaged region of interest. However, the placenta has a complex structure and flow profile, which is insufficiently described using the conventional technique. In this work, we apply curve fitting in each pixel of the CEUS image series in order to quantify haemodynamic parameters in the placenta and surrounding tissue. The methods quantified an increase in mean placental blood volume and relative blood flow from gestational day (GD) 14 to GD18, while the mean transit time of the microbubbles decreased, demonstrating an overall rise in placental perfusion during gestation. The variance of all three parameters increased during gestation, showing that regional differences in perfusion are observable using the pixel-wise TIC approach. Additionally, the high-resolution parametric images show distinct regions of high blood flow developing during late gestation. The developed methods could be applied to assess placental vascular remodelling during the treatment of the pathologies of pregnancy.
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Wang, Yiyan, Yaoyao Dong, Yinghui Fang та ін. "Diethylstilbestrol inhibits human and rat 11β-hydroxysteroid dehydrogenase 2". Endocrine Connections 8, № 7 (2019): 1061–69. http://dx.doi.org/10.1530/ec-19-0288.
Full textAbstract:
Glucocorticoid hormone might cause intrauterine growth restriction. The glucocorticoid-metabolizing enzyme 11β-hydroxysteroid dehydrogenase 2 (HSD11B2) in the placenta eliminates excess levels of glucocorticoids during pregnancy. The aim of the current study was to define the effects of diethylstilbestrol (DES) on HSD11B2 activity in the mammalian placentas and identify its mode of action. Rat and human placental microsomal HSD11B2 were incubated with different concentrations of DES, and IC50 values were determined. The mode of action was analyzed by incubation of DES together with substrates, glucocorticoid and NAD+. DES suppressed rat and human HSD11B2 with IC50 values of 5.33 and 12.62 μM, respectively. DES was a competitive inhibitor of rat and human HSD11B2 when steroid substrates were added, while it was an uncompetitive inhibitor when cofactor NAD+ was exposed. Oral administration of DES (0.5 mg/kg) to the rat delayed the cortisol metabolism in adult female Sprague–Dawley rats, as indicated by the increases in cortisol’s elimination half-life, maximum concentration and area under the curve. In conclusion, DES is a potent HSD11B2 inhibitor, possibly contributing to the intrauterine growth restriction.
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St-Pierre, M. V., T. Stallmach, A. Freimoser Grundschober, et al. "Temporal expression profiles of organic anion transport proteins in placenta and fetal liver of the rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 6 (2004): R1505—R1516. http://dx.doi.org/10.1152/ajpregu.00279.2003.
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Physiological cholestasis linked to immature hepatobiliary transport systems for organic anions occurs in rat and human neonates. In utero, the placenta facilitates vectorial transfer of certain fetal-derived solutes to the maternal circulation for elimination. We compared the ontogenesis of organic anion transporters in the placenta and the fetal liver of the rat to assess their relative abundance throughout gestation and to determine whether the placenta compensates for the late maturation of transporters in the developing liver. The mRNA of members of the organic anion transporting polypeptide (Oatp) superfamily, the multidrug resistance protein (Mrp) family, one organic anion transporter (OAT), and the bile acid carriers Na+-taurocholate cotransporting polypeptide (Ntcp) and bile salt export pump (Bsep) was quantified by real-time PCR. The most abundant placental transporters were Oatp4a1, whose mRNA increased 10-fold during gestation, and Mrp1. Mrp1 immunolocalized predominantly to epithelial cells of the endoplacental yolk sac, suggesting an excretory role that sequesters fetal-derived solutes in the yolk sac cavity, and faintly to the basal syncytiotrophoblast surface. The mRNA levels of Oatp2b1, Mrp3, and Bsep in the placenta exceeded those in the fetal liver until day 20 of gestation, suggesting that the fetus relies on placental clearance of substrates when expression in the developing liver is low. Mrp3 immunolocalized to the epithelium of the endoplacental yolk sac and less abundantly in the labyrinth zone and endothelium of the maternal arteries. The placental expression of Oatp1a1, Oatp1a4, Oatp1a5, Oatp1b2, Oat, Ntcp, Mrp2, and Mrp6 was low.
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Belkacemi, Louiza, Mina Desai, D. Michael Nelson, and Michael G. Ross. "Altered mitochondrial apoptotic pathway in placentas from undernourished rat gestations." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 6 (2011): R1599—R1615. http://dx.doi.org/10.1152/ajpregu.00100.2011.
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Maternal undernutrition (MUN) during pregnancy results in intrauterine growth-restricted (IUGR) fetuses and small placentas. Although reduced fetal nutrient supply has been presumed to be etiologic in IUGR, MUN-induced placental dysfunction may occur prior to detectable fetal growth restriction. Placental growth impairment may result from apoptosis signaled by mitochondria in response to reduced energy substrate. Therefore, we sought to determine the presence of mitochondrial-induced apoptosis under MUN and ad libitum diet (AdLib) pregnancies. Pregnant rats were fed an AdLib or a 50% MUN diet from embryonic day 10 (E10) to E20. At E20, fetuses and placentas from proximal- and mid-horns (extremes of nutrient/oxygen supply) were collected. Right-horn placentas were used to quantify apoptosis. Corresponding left-horn placentas were separated into basal (hormone production) and labyrinth (feto-maternal exchange) zones, and protein expression of the mitochondrial pathway was determined. Our results show that the MUN placentas had significantly increased apoptosis, with lower expression of cytosolic and mitochondrial anti-apoptotic Bcl2 and Bcl-XL, and significantly higher expression of pro-apoptotic Bax and Bak especially in the labyrinth zone. This was paralleled by higher coimmunostaining with the mitochondrial marker manganese superoxide dismutase (MnSOD), indicating transition of pro-apoptotic factors to the mitochondrial membrane. Also, cytosolic cytochrome c and activated caspases-9 and -3 were significantly higher in all MUN. Conversely, peroxisome proliferator-activator receptor-γ (PPARγ), a member of the nuclear receptor family with anti-apoptotic properties, was significantly downregulated in both zones and horns. Our results suggest that MUN during rat pregnancy enhances mitochondria-dependent apoptosis in the placenta, probably due to the downregulation of PPARγ expression.
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Bobrova, Olena, Yevheniia Naumenko, Myroslav Shchetinskyi, et al. "Low-Temperature Storage of Placenta Affects Anti-Inflammatory and Wound Healing Properties of Its Extracts." Problems of Cryobiology and Cryomedicine 32, no. 2 (2022): 144–57. http://dx.doi.org/10.15407/cryo32.02.144.
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Here we have studied the effect of low-temperature storage of the placenta at different temperatures on anti-inflammatory activity of its extracts in cell models of erythrocyte thermohemolysis and adenosine-5’-diphosphate-induced platelet aggregation. The wound-healing effect of cryopreserved placental extracts was also evaluated in rat thermal burn model. When preserving placenta for up to a month, the temperature of storage was shown to cause no significant impact on the percentage of inhibition of erythrocyte thermohemolysis and platelet aggregation by the extracts. Placental storage for three months at –20°C decreased anti-inflammatory activity of its extracts, and led to its complete loss during 6 months. Placental cryopreservation at –196°C enabled to preserve the anti-inflammatory and wound-healing activity. The cryopreserved placenta-derived extracts showed a pronounced positive effect on reparative process at third-degree (B) skin burn injury in rats.
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McMillen, Cynthia M., Devin A. Boyles, Stefan G. Kostadinov, et al. "Congenital Rift Valley fever in Sprague Dawley rats is associated with diffuse infection and pathology of the placenta." PLOS Neglected Tropical Diseases 16, no. 10 (2022): e0010898. http://dx.doi.org/10.1371/journal.pntd.0010898.
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Rift Valley fever (RVF) is a disease of animals and humans associated with abortions in ruminants and late-gestation miscarriages in women. Here, we use a rat model of congenital RVF to identify tropisms, pathologies, and immune responses in the placenta during vertical transmission. Infection of late-gestation pregnant rats resulted in vertical transmission to the placenta and widespread infection throughout the decidua, basal zone, and labyrinth zone. Some pups from infected dams appeared normal while others had gross signs of teratogenicity including death. Histopathological lesions were detected in placenta from pups regardless of teratogenicity, while teratogenic pups had widespread hemorrhage throughout multiple placenta layers. Teratogenic events were associated with significant increases in placental pro-inflammatory cytokines, type I interferons, and chemokines. RVFV displays a high degree of tropism for all placental tissue layers and the degree of hemorrhage and inflammatory mediator production is highest in placenta from pups with adverse outcomes. Given the potential for RVFV to emerge in new locations and the recent evidence of emerging viruses, like Zika and SARS-CoV-2, to undergo vertical transmission, this study provides essential understanding regarding the mechanisms by which RVFV crosses the placenta barrier.
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Hewitt, D. P., P. J. Mark, A. M. Dharmarajan та B. J. Waddell. "274. Placental expression of secreted frizzled related protein (sFRP4) in the rat: association with β-catenin localization and regulation by glucocorticoids". Reproduction, Fertility and Development 17, № 9 (2005): 113. http://dx.doi.org/10.1071/srb05abs274.
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Wnt genes regulate a diverse range of developmental processes including placental development. Activation of the wnt pathway results in nuclear translocation of β-catenin and activation of the TCF/Lef family of transcription factors. The secreted frizzled related proteins (sFRPs) modulate wnt signaling by binding to either the wnt ligand or its transmembrane frizzled receptor. The current study examined the spatial and temporal expression of one of these secreted molecules, sFRP4, in the rat placenta over the final third of pregnancy, and whether associated changes occurred in the expression and localization of β-catenin. The expression of sFRP4 and β-catenin was also analysed in a model of glucocorticoid-induced placental growth restriction. Analysis by quantitative RT-PCR over the final third of pregnancy demonstrated a dramatic increase in sFRP4 mRNA (14-fold, P < 0.001) specifically within the basal zone of the placenta near term. In situ hybridization and immunohistochemistry localized sFRP4 expression primarily to giant trophoblasts of the basal zone. In addition, sFRP4 protein was notably upregulated in association with a restricted nuclear translocation of β-catenin. Maternal dexamethasone treatment (1 μg/mL in drinking water; day 13–22) further increased the expression of sFRP4 mRNA in both the basal (120%, P < 0.05) and labyrinth (285%, P < 0.01) zones of the placenta at day 22 (term = 23 days) compared to untreated controls. These data indicate that sFRP4 expression is increased in the basal zone of the rat placenta, the major site of apoptosis in late pregnancy, and is further stimulated by glucocorticoids. Moreover, the observed inhibition of β-catenin expression and its nuclear translocation suggest that sFRP4 inhibition of wnt signaling in the placenta may contribute to placental apoptosis and ultimately fetal growth restriction.
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Jousset, V., B. Legendre, P. Besnard, N. Segond, A. Jullienne, and J. M. Garel. "Calcitonin-like immunoreactivity and calcitonin gene expression in the placenta and in the mammary gland of the rat." Acta Endocrinologica 119, no. 3 (1988): 443–51. http://dx.doi.org/10.1530/acta.0.1190443.
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Abstract. Recently, the presence of monomeric CT in plasma and milk was reported by others in a lactating woman surgically thyroidectomized. Similarly, the placenta was thought to be a possible source of CT. Since such findings were based exclusively on immunological arguments, we have investigated the CT gene expression in these rat tissues. CT mRNAs were detected by dot-blot hybridization of total RNAs extracted from rat tissues with a 32P-labelled human CT cDNA probe. Subcellular fractions of each tissue were screened for CT-like immunoreactivity using two different antibodies. With one antibody, extracts of the mammary gland and placenta both produced full displacement of labelled human CT from the antiserum and serial dilutions of the extracts gave displacement curves parallel to that of synthetic human CT, which suggests immunological similarity. However, dilution curves were not parallel for the second antibody, and for both antisera, CT-like immunoreactivity was found in all subsellular fractions from nuclei to cytosols. Immunoprecipitation of translation products from poly (A)+RNAs of placenta showed two major bands around 30 kD. Under stringent conditions, the weak hybridization of placental RNAs seen by dot-blot under less stringent conditions disappeared. Northern analyses of total RNAs from the placenta failed to detect mRNA of 1 k base size like in thyroid glands, but hybridization under weak stringent conditions occurred with larger mRNAs (around 4.4 and 2.4 k bases). Immunoprecipitation of translation products from mRNAs of rat mammary glands showed three major bands around 46, 30 and 20 kD. Dot-blot hybridization of total RNAs extracted from mammary glands was also negative. In conelusion, our results suggest that the CT gene is not expressed in the rat placenta and in rat mammary gland, since CT mRNAs were not detected in either tissues.
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Animaw, Zelalem, Kaleab Asres, Selamawit Tadesse, et al. "Teratogenic Evaluation of 80% Ethanol Extract of Embelia schimperi Vatke Fruits on Rat Embryo and Fetuses." Journal of Toxicology 2022 (October 22, 2022): 1–12. http://dx.doi.org/10.1155/2022/4310521.
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Introduction. Embelia schimperi Vatke (family Myrsinaceae) is a commonly consumed anthelminthic plant in Ethiopia. The plant has significant efficacy in treating intestinal worms. However, there are limited data about the safety/toxicity of the plant. Moreover, the teratogenic effect of the plant is not yet well studied despite significant number of Ethiopian mothers consuming herbal medication during their pregnancy. Purpose. This study aimed to evaluate the teratogenic effect of the hydroalcoholic extract of E. schimperi fruit on rat embryos and fetuses. Methods. Pregnant albino Wistar rats were treated with 80% hydroalcoholic fruit extract of E. schimperi at 250 mg/kg, 500 mg/kg, and 1000 mg/kg dosage, whilst the controls were pair-fed and ad libitum groups. Maternal food intake, maternal weight gain, number of implantations, number of prior resorptions, fetal viability, fetal weight, fetal and embryonic crown-ramp length, placental weight, placental gross morphology and histopathology of placental tissue, number of somites, embryonic system, gross/visceral morphological malformations, and ossification centers were evaluated as teratogenicity indices. Results. The crude extract of E. schimperi did not exhibit a significant difference in most developmental indices including the development of a circulatory system, nervous system, and musculoskeletal systems among treated animals and the controls. However, histopathological evaluation of placentas from the treatment groups showed that inflammatory reactions and calcifications compared to the pair-fed and ad libitum controls. Conclusion. Administration of the 80% hydroalcoholic extract of E. schimperi fruit during the period of organogenesis in rats did not show a significant toxic effect on embryonic and fetal developmental indices. However, it might affect the structural integrity of the placenta as it is evidenced by inflammatory reactions and calcifications of decidua basalis of rat placenta.
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Choudhury, S., M. Reyes, NN Drever, et al. "ID: 105: COMPARISON OF PLACENTAL AND PLASMA SOLUBLE (PRO)RENIN RECEPTOR IN NORMAL AND PREECLAMPTIC PREGNANCY." Journal of Investigative Medicine 64, no. 4 (2016): 958.1–958. http://dx.doi.org/10.1136/jim-2016-000120.96.
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ObjectivePreeclampsia (preE), a syndrome of hypertension and proteinuria. Most recently it was demonstrated that high circulating levels of soluble (pro) renin receptor s(P)RR at delivery were associated with preE. In this study the placental expression of (P)RR were evaluated in preE patients and in a rat model of preE as well as in nonhuman primates. We also evaluated the circulatory levels of s(P)RR.Study Design(1) Placental samples were collected from 20 NP and 20 preE consenting patients in an IRB approved prospective study. (2) An established rat model of preE and NP rats (n=10 each) were used. (3) The placental samples from squirrel monkey (NP; n=10) and owl monkey (both early and term, NP, n=1) were collected. The (P)RR expression were measured both by western blotting (WB) and Immunohistochemistry (IHC) using anti-ATP6IP2. The levels of serum s(P)RR were measured by ELISA.ResultsThe placental expression of (P)RR were higher (p<0.05) in preE compared to NP both in patients and rat model. The s(P)RR levels were higher in preE (preE patients: 29.2±4.5; PDS rats: 16.9±1.9 ng/mL) compared to NP (NP human: 19.3±4.2; NP rats: 10.4±3.7 ng/mL). The early placenta of owl monkey expressed higher (P)RR compared to term and were expressed in squirrel monkey placentas.ConclusionsThese data suggest that increased expression of (P)RR in the placenta are related to the occurrence of preE in both patients and rat models. These data also reconfirmed that the high level of circulatory s(P)RR is associated with preE. The higher expression of (P)RR in early owl monkey in compare to term placenta suggests that the (P)RR is important for normal placental development. The expression of (P)RR in nonhuman primates reveals the approach of future studies on owl monkey and squirrel monkey preE models.
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Ni, Wensi, Haoxuan Gao, Bing Wu, et al. "Gestational Exposure to Cyfluthrin through Endoplasmic Reticulum (ER) Stress—Mediated PERK Signaling Pathway Impairs Placental Development." Toxics 10, no. 12 (2022): 733. http://dx.doi.org/10.3390/toxics10120733.
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Cyfluthrin, a typical type II pyrethroid pesticide, is widely used in house hygiene and agricultural pest control. Several epidemiological investigations have found that maternal pyrethroid exposure is connected to adverse pregnancy outcomes. However, the underlying mechanisms remain to be elucidated. Thus, we evaluated the effect of cyfluthrin exposure during pregnancy on placenta development in vivo. In the current study, Pregnant SD rats were randomly divided into four groups and administered 6.25, 12.5, and 25 mg/kg body weight cyfluthrin or an equivalent volume of corn oil by gavage from GD0 to GD19. The results have shown that gestational exposure to cyfluthrin exerted no effect on the fetal birth defect, survival to PND4, or fetal resorption and death. However, live fetuses and implantation sites significantly decreased in the high-dose cyfluthrin-treated group. Moreover, a significant reduction in placenta weight and diameter was observed in rats. Correspondingly, the fetal weight and crown-rump length from dams exposed to cyfluthrin were reduced. Cyfluthrin-treat groups, the total area of the placenta, spongiotrophoblast area, and labyrinth area had abnormal changes. Meanwhile, the area of blood sinusoid and CD34-positive blood vessel numbers in the placenta were considerably reduced, as well as abnormal expression of placental pro-angiogenic and anti-angiogenic factors in dams exposed to cyfluthrin. Further observation by transmission electron microscopy revealed significant changes in the ultrastructure of the medium-dose and high-dose groups. Additional experiments showed gestational exposure to cyfluthrin inhibited proliferation and induced apoptosis of placentas, as decreased PCNA-positive cells and increased TUNEL-positive cells. Furthermore, western blot and qPCR analysis revealed that gestational exposure to medium-dose and high-dose cyfluthrin increased the expression of GRP78, and three downstream mRNA and proteins (p-eIF2α, ATF4, and CHOP) of the PERK signaling, indicating that endoplasmic reticulum (ER) stress-mediated PERK/eIF2α/ATF4/CHOP signaling pathway in rat placentas was activated. Our study demonstrated that gestational exposure to cyfluthrin leads to placental developmental disorder, which might be associated with ER stress-mediated PERK signaling pathway.
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Takizawa, Tatsuya, Hiroshi Yoshikawa, Miho Yamada, and Hidetoshi Morita. "Expression of nitric oxide synthase isoforms and detection of nitric oxide in rat placenta." American Journal of Physiology-Cell Physiology 282, no. 4 (2002): C762—C767. http://dx.doi.org/10.1152/ajpcell.00101.2001.
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Nitric oxide (NO) production in the rat placenta was monitored and quantified by electron paramagnetic resonance (EPR) spectroscopy with hemoglobin and an Fe- N-(dithiocarboxy)sarcosine (DTCS) complex as NO-trapping reagents. Expression of nitric oxide synthase (NOS) isoforms was also examined by quantitative RT-PCR analysis. The EPR spectrum of the placenta with hemoglobin trapping showed a three-line hyperfine structure ( g = 2.008 and a = 1.66-mT). The EPR signal was diminished after the placenta was homogenized or the NOS inhibitor l-NAME was administered to pregnant rats. Therefore, the specific signal was definitely identified as being derived from endogenous NO spin-trapped by hemoglobin, and the EPR spectrum showed that the NO adduct existed as a pentacoordinate α-NO heme species. The EPR spectrum of the placenta with Fe-DTCS trapping showed a triplet signal ( g = 2.038) derived from an NO-Fe-DTCS complex. The height of the triplet signal did not vary significantly with gestational stage during the last few days of gestation. At the gestational stages examined, the level of NOS II mRNA expression was significantly higher than that of NOS III mRNA. NOS II expression in term ( day 21.5) placenta was significantly increased compared with that in preterm ( day 19.5) placenta ( P < 0.01, n = 4 or 5). These results suggest that NOS II is the predominant producer of NO in the placenta and that NOS II-generated NO plays significant roles in the maintenance of placental functions immediately before birth.
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Jones, M. L., P. J. Mark, and B. J. Waddell. "215. Placental expression of uncoupling protein-2 is reduced by glucocorticoid treatment in late pregnancy: implications for placental oxidative stress." Reproduction, Fertility and Development 20, no. 9 (2008): 15. http://dx.doi.org/10.1071/srb08abs215.
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Placental oxidative stress plays a key role in the pathophysiology of placenta-related disorders in humans, most notably in preeclampsia (PE) and intrauterine growth restriction (IUGR). Protection from oxidative stress is provided by antioxidant enzymes including superoxide dismutase-1 and 2 (SOD-1 and –2) and catalase (CAT), which convert reactive oxygen species (ROS) to inert products. It has also been proposed that uncoupling protein-2 (UCP2) may limit oxidative stress by reducing ROS production, but little is known of UCP2 expression in placenta. Here we measured placental UCP2, SOD-1, SOD-2 and CAT mRNA expression (by qRT–PCR) in normal gestation and after glucocorticoid-induced IUGR. The latter was included because glucocorticoids can increase oxidative stress in other tissues, and placental glucocorticoid exposure is elevated in both PE and IUGR. Placentas were collected on days 16 and 22 of normal pregnancy (term = day 23) and on day 22 after dexamethasone treatment (0.75 mg/mL in drinking water from day 13). The two morphologically-distinct regions of the placenta, the junctional (JZ) and labyrinth (LZ) zones, were analysed separately because effectively all growth occurs in the LZ over this period. Expression of UCP2 in LZ exceeded that in JZ (P < 0.001) and increased in both zones between days 16 and 22 (LZ: 2.0-fold; JZ: 3.2-fold). Dexamethasone treatment reduced UCP2 in LZ (44%; P < 0.05) but not in JZ. SOD1 and SOD2 increased with gestational age in LZ (P < 0.01) and JZ (P < 0.05), but neither were affected by dexamethasone. CAT expression was higher (2.4-fold, P < 0.001) in LZ compared with JZ but did not change with gestational age or dexamethasone. In summary, these data suggest that endogenous protection against oxidative stress increases in the rat placenta during late pregnancy. Moreover, this protection may be compromised by reduced placental UCP2 expression in a model of glucocorticoid-induced IUGR.
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Story, C. M., J. E. Mikulska, and N. E. Simister. "A major histocompatibility complex class I-like Fc receptor cloned from human placenta: possible role in transfer of immunoglobulin G from mother to fetus." Journal of Experimental Medicine 180, no. 6 (1994): 2377–81. http://dx.doi.org/10.1084/jem.180.6.2377.
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The acquisition of maternal antibodies is critical for immunologic defense of the newborn. In humans, maternal IgG is actively transported across the placenta. The receptor responsible for this transport has not been identified definitively. We report the isolation from a placental cDNA library of clones encoding the alpha-chain of an immunoglobulin G (IgG)-Fc receptor (hFcRn) that resembles a class I major histocompatibility complex antigen. The DNA and predicted amino acid sequences are very similar to those of the neonatal rat and mouse intestinal Fc receptors, rFcRn and mFcRn. These receptors mediate transport of maternal IgG from milk to the blood-stream of the suckling rat or mouse. Like rat and mouse FcRn, hFcRn binds IgG preferentially at low pH, which may imply that IgG binds hFcRn in an acidic intracellular compartment during transport across the placenta.
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Burton, P. J., та B. J. Waddell. "11β-Hydroxysteroid dehydrogenase in the rat placenta: developmental changes and the effects of altered glucocorticoid exposure". Journal of Endocrinology 143, № 3 (1994): 505–13. http://dx.doi.org/10.1677/joe.0.1430505.
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Abstract The enzyme 11β-hydroxysteroid dehydrogenase (11β-HSD) catalyses the interconversion of corticosterone, the major glucocorticoid of the rat, and the biologically-inactive 11-dehydrocorticosterone. In the placenta, 11β-HSD is thought to regulate glucocorticoid transport between maternal and fetal compartments, and may also affect the local action of glucocorticoids. The present study assessed whether 11β-dehydrogenase (corticosterone to 11-dehydrocorticosterone) and 11-oxoreductase (11-dehydrocorticosterone to corticosterone) activities are both present in rat placenta, and whether these activities change with advancing pregnancy. Enzyme activity was estimated on days 16, 19 and 22 of pregnancy (term=day 23) in placental fragments incubated for 6 h with either [3H]corticosterone or [3H] 11-dehydrocorticosterone. The percentage conversion of these substrates to [3H] 11-dehydrocorticosterone and [3H] corticosterone, respectively, were determined at the end of the incubation. Both 11-oxoreductase and 11β-dehydrogenase activities were clearly evident in placental tissue fragments, and while 11-oxoreductase activity declined with advancing pregnancy (P<0·01), 11β-dehydrogenase activity increased (P<0·01). Thus, 11-oxoreductase exceeded (P<0·05) 11β-dehydrogenase at day 16, but thereafter activities were similar. These changes do not appear to be glucocorticoid-induced, since pretreatment of rats with either metyrapone or dexamethasone acetate from day 15 of pregnancy did not affect placental 11β-HSD on day 22. To allow comparison with earlier studies, estimates of 11β-HSD were also made in placental homogenates at each stage of pregnancy. In contrast to observations in placental fragments, 11β-dehydrogenase was always the dominant reaction in homogenates, presumably due to the loss of 11-oxoreductase activity following tissue homogenisation. These data demonstrate that net 11β-dehydrogenase activity in the rat placenta increases towards term, thereby increasing the capacity for placental inactivation of active glucocorticoid. This pattern of 11β-HSD is consistent with reduced transfer of active glucocorticoid between the mother and fetus near term, and thus should promote independence of their hypothalamic-pituitary-adrenal axes. Journal of Endocrinology (1994) 143, 505–513
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Rodda, C. P., M. Kubota, J. A. Heath, et al. "Evidence for a novel parathyroid hormone-related protein in fetal lamb parathyroid glands and sheep placenta: comparisons with a similar protein implicated in humoral hypercalcaemia of malignancy." Journal of Endocrinology 117, no. 2 (1988): 261–71. http://dx.doi.org/10.1677/joe.0.1170261.
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ABSTRACT Parathyroid hormone (PTH)-like bioactivity, assayed as adenylate cyclase response in UMR 106-01 osteogenic sarcoma cells, was present in extracts of sheep fetal and maternal parathyroid glands and placenta. Preincubation of extracts with PTH(1–34) antiserum inhibited approximately 40% of the bioactivity in fetal parathyroid extracts, 50% in maternal parathyroid extracts, but only 10% of the bioactivity in the placental extract. Partial purification of placental extracts by chromatography yielded fractions containing PTH-like bioactivity which were similar in behaviour to that of PTH-related protein (PTHrP) from a human lung cancer cell line (BEN). An antiserum against synthetic PTHrP(1–16) partially inhibited the bioactivity of the placental extract and synthetic PTHrP(1–34), but had no effect on the bioactivity of bovine PTH(1–34) or bovine PTH(1– 84). The placental PTH-like bioactivity was higher in mid- than in late gestation. Fetal parathyroid glands contained the highest PTH-like bioactivity. Thyroparathyroidectomy of one fetal twin lamb in each of 16 ewes between 110 and 125 days of gestation resulted in decreases of the plasma calcium concentration and reversal of the placental calcium gradient that existed between the ewe and the intact fetus. Perfusion of the placenta of each twin in anaesthetized ewes was carried out sequentially with autologous fetal blood in the absence of the exsanguinated fetus. The plasma calcium concentration in the blood perfusing the placenta of each twin increased, but reached a plateau at a lower concentration in the perfusing blood of thyroparathyroidectomized fetuses than in that of the intact fetuses. Addition of extracts of fetal parathyroid glands or of partially purified PTHrP resulted in further increases in plasma calcium in the autologous blood perfusing the placentae of thyroparathyroidectomized fetuses, but addition of bovine PTH(1–84) or rat PTH(1–34) had no effect. The presence of this PTH-like protein in the fetal parathyroid gland and placenta may contribute to the relative hypercalcaemia of the fetal lamb. This protein, which is similar to PTHrP associated with humoral hypercalcaemia of malignancy, stimulates the placental calcium pump responsible for maintaining a relative fetal hypercalcaemia during gestation. J. Endocr. (1988) 117, 261–271
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Ruis, Matthew T., Kylie D. Rock, Samantha M. Hall, Brian Horman, Heather B. Patisaul, and Heather M. Stapleton. "PBDEs Concentrate in the Fetal Portion of the Placenta: Implications for Thyroid Hormone Dysregulation." Endocrinology 160, no. 11 (2019): 2748–58. http://dx.doi.org/10.1210/en.2019-00463.
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Abstract During pregnancy, the supply of thyroid hormone (TH) to the fetus is critically important for fetal growth, neural development, metabolism, and maintenance of pregnancy. Additionally, in cases where maternal and placental TH regulation is significantly altered, there is an increased risk of several adverse pregnancy outcomes. It is unclear what may be disrupting placental TH regulation; however, studies suggest that environmental contaminants, such as polybrominated diphenyl ethers (PBDEs), could be playing a role. In this study, Wistar rats were gestationally exposed to a mixture of PBDEs for 10 days. THs and PBDEs were quantified in paired maternal serum, dissected placenta, and fetuses, and mRNA expression of transporters in the placenta was assessed. Significantly higher concentrations of PBDEs were observed in the fetal portion of the placenta compared with the maternal side, suggesting that PBDEs are actively transported across the interface. PBDEs were also quantified in 10 recently collected human maternal and fetal placental tissues; trends paralleled observations in the rat model. We also observed an effect of PBDEs on T3 levels in dam serum, as well as suggestive changes in the T3 levels of the placenta and fetus that varied by fetal sex. mRNA expression in the placenta also significantly varied by fetal sex and dose. These observations suggest the placenta is a significant modifier of fetal exposures, and that PBDEs are impacting TH regulation in a sex-specific manner during this critical window of development.
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MacManus, J. P., D. C. Watson, and M. Yaguchi. "The purification and complete amino acid sequence of the 9000-Mr Ca2+-binding protein from rat placenta. Identity with the vitamin D-dependent intestinal Ca2+-binding protein." Biochemical Journal 235, no. 2 (1986): 585–95. http://dx.doi.org/10.1042/bj2350585.
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A 9000-Mr Ca2+-binding protein was isolated from rat placenta and purified to homogeneity by h.p.l.c. procedures. The complete amino acid sequence was established for the 78-residue placental protein. A sequence analysis of a minor component of the rat intestinal Ca2+-binding protein (residues 4-78) and a tryptic peptide (residues 55-74), both purified by h.p.l.c., showed both proteins to be identical. Thus this placental 9000-Mr Ca2+-binding protein is the same gene product as the intestinal Ca2+-binding protein whose synthesis is dependent on vitamin D.
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Rahardjo, Bambang, Kunawati Tungga Dewi, Anita Dwi Rahmawati, Fauqo Wildatil Jannah, Mukhamad Nooryanto, and Anin Indriani. "Effect of Pravastatin on eNOS and PECAM-1 Expression in the Placenta of Pre-Eclampsia Rat (Rattus norvegicus) Model." Asian Journal of Health Research 1, no. 2 (2022): 12–18. http://dx.doi.org/10.55561/ajhr.v1i2.44.
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Introduction: Preeclampsia has two stages: improper placental and maternal circulation. Abnormal trophoblast invasion causes uteroplacental ischemia and hypoxia. Ischemia in the placenta produces endothelial cell dysfunction, which is defined by a change in endothelial cell activity to a reduced ability to vasodilate (decreased eNOS) and prothrombotic conditions (decreased PECAM-1). Reduced maternal eNOS activity and PECAM-1 can cause preeclampsia. Pravastatin is the statin class's most hydrophilic medication, and it limits placental transfer. Pravastatin can reduce endothelial dysfunction by targeting pleiotropic effects in pregnancy. The aim was to show the effects of pravastatin on the eNOS and PECAM-1 expression in the placenta of preeclampsia rat model.
 Materials and Methods: This is a true experimental study with only a post-test and a control group design. The sample was biological material in the form of placental tissue from a pravastatin-treated preeclampsia rat model (using L-NAME exposure). This research was divided into five groups, each with five samples. The parameters studied were eNOS and PECAM-1 expression.
 Results: The Shapiro-Wilk test result was significant (p>0.05). Annova tests on eNOS (p=0.000) and PECAM-1 expression (p=0.000) confirmed the hypothesis. The Tukey test showed significant differences in eNOS (sig. 0.001) and PECAM-1 (sig. 0.000) expression between normal and preeclampsia rats. Positive controls and treatment groups P1, P2, and P3 all showed significant changes in eNOS and PECAM-1 expression. Pravastatin dose considerably increased eNOS (p=0.015; r=0.536) and PECAM-1 (p=0.000; r=0.734) expression..
 Conclusion: Pravastatin has been shown to increase eNOS and PECAM-1 expression in the placenta of preeclampsia rat model.
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Phuthong, Sophida, Cynthia Guadalupe Reyes-Hernández, Pilar Rodríguez-Rodríguez, et al. "Sex Differences in Placental Protein Expression and Efficiency in a Rat Model of Fetal Programming Induced by Maternal Undernutrition." International Journal of Molecular Sciences 22, no. 1 (2020): 237. http://dx.doi.org/10.3390/ijms22010237.
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Fetal undernutrition programs cardiometabolic diseases, with higher susceptibility in males. The mechanisms implicated are not fully understood and may be related to sex differences in placental adaptation. To evaluate this hypothesis, we investigated placental oxidative balance, vascularization, glucocorticoid barrier, and fetal growth in rats exposed to 50% global nutrient restriction from gestation day 11 (MUN, n = 8) and controls (n = 8). At gestation day 20 (G20), we analyzed maternal, placental, and fetal weights; oxidative damage, antioxidants, corticosterone, and PlGF (placental growth factor, spectrophotometry); and VEGF (vascular endothelial growth factor), 11β-HSD2, p22phox, XO, SOD1, SOD2, SOD3, catalase, and UCP2 expression (Western blot). Compared with controls, MUN dams exhibited lower weight and plasma proteins and higher corticosterone and catalase without oxidative damage. Control male fetuses were larger than female fetuses. MUN males had higher plasma corticosterone and were smaller than control males, but had similar weight than MUN females. MUN male placenta showed higher XO and lower 11β-HSD2, VEGF, SOD2, catalase, UCP2, and feto-placental ratio than controls. MUN females had similar feto-placental ratio and plasma corticosterone than controls. Female placenta expressed lower XO, 11β-HSD2, and SOD3; similar VEGF, SOD1, SOD2, and UCP2; and higher catalase than controls, being 11β-HSD2 and VEGF higher compared to MUN males. Male placenta has worse adaptation to undernutrition with lower efficiency, associated with oxidative disbalance and reduced vascularization and glucocorticoid barrier. Glucocorticoids and low nutrients may both contribute to programming in MUN males.
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Situmorang, Putri Cahaya, Syafruddin Ilyas, Doni Aldo Samuel Siahaan та ін. "Effect of Rhodomyrtus tomentosa Hassk. on HIF1α and VEGF expressions on hypertension placental". Journal of Pharmacy & Pharmacognosy Research 10, № 6 (2022): 1076–86. http://dx.doi.org/10.56499/jppres22.1517_10.6.1076.
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Context: HIF1α and VEGF are proteins marker oxidative stress and a decrease in placental growth factor (PlGF). Decreasing of HIF1α and VEGF in rats displayed poor trophoblast differentiation, placental abnormalities, and fetal mortality. Rhodomyrtus tomentosa is a flowering plant in the Myrtaceae family that has the potential to be a source of health-promoting chemicals. Aims: To analyze HIF1α and VEGF in serum and hypertension placental tissue after giving Rhodomyrtus tomentosa (RHO) leaves extract. Methods: Six treatments were given to the rats that were identified as being pregnant and pregnant rats with hypertension were given RHO with three doses: (a) normal pregnant rats (control); (b) hypertensive rats; (c) hypertensive rats + 100 mg/kg BW of RHO; (d) hypertensive rats +200 mg/kg BW of RHO; and (e) hypertensive rats + 400 mg/kg BW of RHO and (f) hypertensive rats + nifedipine. Under ketamine anesthesia, pregnant rats were removed on their 20th day of gestation. Immunohistochemistry and ELISA were used to assess HIF1α and VEGF protein expression. Results: There was a significant difference (p<0.01) in the expression of HIF1α and VEGF in the labyrinthine zone and yolk sac of the rat placenta between the normal (C-) and hypertensive (C+) groups. HIF1α and VEGF expression decreased when RHO was administered at doses ranging from 100 to 400 mg/kg BW. However, there was no significant change (p>0.05) in VEGF expression in the basal zone of the rat placenta across all groups. Conclusions: Rhodomyrtus tomentosa leaves extract decreases HIF1α and VEGF expressions in serum and repairs the tissue of the placenta's labyrinth, basal, and yolk sacs.
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Zhang, KeKe, Min Hu, Lin Zhang, Qiong Zhang, and Yinping Huang. "The Effect of BML-111 in Preeclampsia Rat Model Induced by the Low Dose of Cadmium Chloride." American Journal of Perinatology Reports 09, no. 03 (2019): e201-e208. http://dx.doi.org/10.1055/s-0039-1693016.
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Aim This article determines the optimal time and dose of cadmium chloride (CdCl2) injected to pregnant rat to establish experimental preeclampsia (PE) model. In addition, the therapeutic potential of BML-111, a lipoxin A4 analogue, in the CdCl2-induced PE model was also evaluated. Methods Peritoneal injection of two dose of CdCl2 for successive 6 days was tested in the pregnant rats starting from various gestational days (GDs). During this process, the systolic blood pressure and the body weight of pregnant rats and neonatal rats were monitored. The pathological changes of the placenta and kidney were evaluated by hematoxylin and eosin staining. The phosphorylation of extracellular signal-regulated kinase 1/2 and signal transducer and activator of transcription 3 in the placentas was detected by Western blot, and the messenger ribonucleic acid expression of interleukin (IL)-6, tumor necrosis factor-α, and IL-10 in the placentas were detected by real-time polymerase chain reaction. BML-111 at the dose of 1 mg/kg/day was peritoneally injected into the rat after establishing the PE model to test its therapeutic potential. Results In the present study, we successfully established the PE model in pregnant rats by intraperitoneally injection of CdCl2 at the dose of 0.125 mg/kg/day from GD 9 to 14. We recapitulated multiple features of clinical PE in CdCl2-induced rat, including high blood pressure, renal dysfunction, and inflammatory response in placenta. Furthermore, treatment with BML-111 significantly relieved multiple features in our PE rat model. Conclusions BML-111 has a potential therapeutic effect in pregnant rats with CdCl2-induced PE, which appears to be mediated through inhibition of inflammatory processes in the placenta.
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Bokar, J. A., R. A. Keri, T. A. Farmerie, et al. "Expression of the glycoprotein hormone alpha-subunit gene in the placenta requires a functional cyclic AMP response element, whereas a different cis-acting element mediates pituitary-specific expression." Molecular and Cellular Biology 9, no. 11 (1989): 5113–22. http://dx.doi.org/10.1128/mcb.9.11.5113-5122.1989.
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The single-copy gene encoding the alpha subunit of glycoprotein hormones is expressed in the pituitaries of all mammals and in the placentas of only primates and horses. We have systematically analyzed the promoter-regulatory elements of the human and bovine alpha-subunit genes to elucidate the molecular mechanisms underlying their divergent patterns of tissue-specific expression. This analysis entailed the use of transient expression assays in a chorionic gonadotropin-secreting human choriocarcinoma cell line, protein-DNA binding assays, and expression of chimeric forms of human or bovine alpha subunit genes in transgenic mice. From the results, we conclude that placental expression of the human alpha-subunit gene requires a functional cyclic AMP response element (CRE) that is present as a tandem repeat in the promoter-regulatory region. In contrast, the promoter-regulatory region of the bovine alpha-subunit gene, as well as of the rat and mouse genes, was found to contain a single CRE homolog that differed from its human counterpart by a single nucleotide. This difference substantially reduced the binding affinity of the bovine CRE homolog for the nuclear protein that bound to the human alpha CRE and thereby rendered the bovine alpha-subunit promoter inactive in human choriocarcinoma cells. However, conversion of the bovine alpha CRE homolog to an authentic alpha CRE restored activity to the bovine alpha-subunit promoter in choriocarcinoma cells. Similarly, a human but not a bovine alpha transgene was expressed in placenta in transgenic mice. Thus, placenta-specific expression of the human alpha-subunit gene may be the consequence of the recent evolution of a functional CRE. Expression of the human alpha transgene in mouse placenta further suggests that evolution of placenta-specific trans-acting factors preceded the appearance of this element. Finally, in contrast to their divergent patterns of placental expression, both the human and bovine alpha-subunit transgenes were expressed in mouse pituitary, indicating differences in the composition of the enhancers required for pituitary- and placenta-specific expression.