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1
Assad, R. S., F. Y. Lee, and F. L. Hanley. "Placental compliance during fetal extracorporeal circulation." Journal of Applied Physiology 90, no. 5 (May 1, 2001): 1882–86. http://dx.doi.org/10.1152/jappl.2001.90.5.1882.
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The fetus requires large amounts of volume when weaning from cardiac bypass. This suggests that placental vasculature can act as a large capacitor in the fetal circulation. To assess placental compliance of fetal lambs, seven isolated in situ lamb placentas were placed on extracorporeal circulation. Umbilical artery blood flow was varied from 0 to 350 ml · min−1· kg fetal wt−1. Because the extracorporeal circuit is a closed system, volume changes in the placenta induced by umbilical artery pressure changes were measured from reciprocal volume changes in the reservoir. There was a wide range of change in absolute volume of blood within the fetal placental compartment (216.4 ± 29.3 ml). Placental compliance was linear over the entire range of pressure changes exerted on the placental vasculature ( r2= 0.83, P = 0.0001). This indicates that the placenta is a unique and sensitive capacitor in the fetal circulation. This information is important clinically because it establishes that aggressive resuscitation of the fetus using volume may be necessary when weaning the fetus from cardiac bypass.
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Vaughan, Owen R., Fredrick Thompson, Ramón A. Lorca, Colleen G. Julian, Theresa L. Powell, Lorna G. Moore, and Thomas Jansson. "Effect of high altitude on human placental amino acid transport." Journal of Applied Physiology 128, no. 1 (January 1, 2020): 127–33. http://dx.doi.org/10.1152/japplphysiol.00691.2019.
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Women residing at high altitudes deliver infants of lower birth weight than at sea level. Birth weight correlates with placental system A-mediated amino acid transport capacity, and severe environmental hypoxia reduces system A activity in isolated trophoblast and the mouse placenta. However, the effect of high altitude on human placental amino acid transport remains unknown. We hypothesized that microvillous membrane (MVM) system A and system L amino acid transporter activity is lower in placentas of women living at high altitude compared with low-altitude controls. Placentas were collected at term from healthy pregnant women residing at high altitude (HA; >2,500 m; n = 14) or low altitude (LA; <1,700 m; n = 14) following planned, unlabored cesarean section. Birth weight, but not placenta weight, was 13% lower in HA pregnancies (2.88 ± 0.11 kg) compared with LA (3.30 ± 0.07 kg, P < 0.01). MVM erythropoietin receptor abundance, determined by immunoblot, was greater in HA than in LA placentas, consistent with lower placental oxygen levels at HA. However, there was no effect of altitude on MVM system A or L activity, determined by Na+-dependent [14C]methylaminoisobutyric acid uptake and [3H]leucine uptake, respectively. MVM abundance of glucose transporters (GLUTs) 1 and 4 and basal membrane GLUT4 were also similar in LA and HA placentas. Low birth weights in the neonates of women residing at high altitude are not a consequence of reduced placental amino acid transport capacity. These observations are in general agreement with studies of IUGR babies at low altitude, in which MVM system A activity is downregulated only in growth-restricted babies with significant compromise. NEW & NOTEWORTHY Babies born at high altitude are smaller than at sea level. Birth weight is dependent on growth in utero and, in turn, placental nutrient transport. We determined amino acid transport capacity in placentas collected from women resident at low and high altitude. Altitude did not affect system A amino acid transport across the syncytiotrophoblast microvillous membrane, suggesting that impaired placental amino acid transport does not contribute to reduced birth weight in this high-altitude population.
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Taher, Shèdy, Yamilette Borja, Lucía Cabanela, Vincent J. Costers, Morgan Carson-Marino, Julie C. Bailes, Biswadeep Dhar, et al. "Cholecystokinin, gastrin, cholecystokinin/gastrin receptors, and bitter taste receptor TAS2R14: trophoblast expression and signaling." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 316, no. 5 (May 1, 2019): R628—R639. http://dx.doi.org/10.1152/ajpregu.00153.2018.
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We investigated expression of cholecystokinin (CCK) in humans and mice, and the bitter taste receptor TAS2R14 in the human placenta. Because CCK and gastrin activate the CCKBR receptor, we also explored placental gastrin expression. Finally, we investigated calcium signaling by CCK and TAS2R14. By RT-PCR, we found CCK/Cck and GAST/Gast mRNA expression in both normal human and mouse placentas, as well as in human trophoblast cell lines (TCL). Although both Cckar and – br mRNA were expressed in the mouse placenta, only CCKBR mRNA was detected in the human placenta and TCL. mRNA expression for TAS2R14 was also observed in the human placenta and TCL. Using immunohistochemistry, CCK protein was localized to the syncytiotrophoblast (ST) and extravillous trophoblast (EVT) in the human term placenta, and to trophoblast glycogen cells in mouse and human placentas. Gastrin and TAS2R14 proteins were also observed in ST and EVT of the human placenta. Both sulfated and nonsulfated CCK elicited a comparable rise in intracellular calcium in TCL, consistent with CCKBR expression. Three TAS2R14 agonists, flufenamic acid, chlorhexidine, and diphenhydramine, also evoked rises in intracellular calcium in TCL. These results establish CCK, gastrin, and their receptor(s) in both human and mouse placentas, and TAS2R14 in the human placenta. Both CCK and TAS2R14 agonists increased intracellular calcium in human TCL. Although the roles of these ligands and receptors, and their potential cross talk in normal and pathological placentas, are currently unknown, this study opens new avenues for placental research.
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Rampon, Christine, Stéphanie Bouillot, Adriana Climescu-Haulica, Marie-Hélène Prandini, Francine Cand, Yves Vandenbrouck, and Philippe Huber. "Protocadherin 12 deficiency alters morphogenesis and transcriptional profile of the placenta." Physiological Genomics 34, no. 2 (July 2008): 193–204. http://dx.doi.org/10.1152/physiolgenomics.00220.2007.
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Protocadherins are transmembrane proteins exhibiting homophilic adhesive activities through their extracellular domain. Protocadherin 12 ( Pcdh12) is expressed in angiogenic endothelial cells, mesangial cells of kidney glomeruli, and glycogen cells of the mouse placenta. To get insight into the role of this protein in vivo, we analyzed PCDH12-deficient mice and investigated their placental phenotype. The mice were alive and fertile; however, placental and embryonic sizes were reduced compared with wild-type mice. We observed defects in placental layer segregation and a decreased vascularization of the labyrinth associated with a reduction in cell density in this layer. To understand the molecular events responsible for the phenotypic alterations observed in Pcdh12−/− placentas, we analyzed the expression profile of embryonic day 12.5 mutant placentas compared with wild-type placentas, using pangenomic chips: 2,289 genes exhibited statistically significant changes in expressed levels due to loss of PCDH12. Functional grouping of modified genes was obtained by GoMiner software. Gene clusters that contained most of the differentially expressed genes were those involved in tissue morphogenesis and development, angiogenesis, cell-matrix adhesion and migration, immune response, and chromatin remodeling. Our data show that loss of PCDH12 leads to morphological alterations of the placenta and to notable changes in its gene expression profile. Specific genes emerging from the microarray screen support the biological modifications observed in PCDH12-deficient placentas.
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Gibbens, Jacob, Shauna-Kay Spencer, Lucia Solis, Teylor Bowles, Patrick B. Kyle, Jamie L. Szczepanski, John Polk Dumas, Reanna Robinson, and Kedra Wallace. "Fas ligand neutralization attenuates hypertension, endothelin-1, and placental inflammation in an animal model of HELLP syndrome." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 319, no. 2 (August 1, 2020): R195—R202. http://dx.doi.org/10.1152/ajpregu.00272.2019.
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Neutralization of FasL is linked to suppression of hypertension, placental inflammation, and endothelin system activation in an animal model of hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome. During HELLP syndrome the placenta has been reported to serve as the primary source of Fas ligand (FasL), which has an impact on inflammation and hypertension during pregnancy and is dysregulated in women with severe preeclampsia and HELLP syndrome. We hypothesize that neutralization of FasL during pregnancy in an animal model of HELLP syndrome decreases inflammation and placental apoptosis, improves endothelial damage, and improves hypertension. On gestational day (GD) 12, rats were chronically infused with placental antiangiogenic factors sFlt-1 and sEng to induce HELLP syndrome. To neutralize FasL, MFL4 or FasL antibody was infused into a subset of HELLP or normal pregnant rats on GD13. IgG infusion into another group of NP and HELLP rats on GD13 was used as a control for FasL antibody, and all rats were euthanized on GD19 after blood pressure measurement. Plasma and placentas were collected to assess inflammation, apoptosis, and the degree of placental debris activation of endothelial cells. Administration of MFL4 to HELLP rats significantly decreased blood pressure compared with untreated HELLP rats and HELLP rats infused with IgG and improved the biochemistry of HELLP syndrome. Both circulating and placental FasL were significantly attenuated in response to MFL4 infusion, as were levels of placental and circulating TNFα when compared with untreated HELLP rats and HELLP rats infused with IgG. Endothelial cells exposed to placental debris and media from HP + MFL4 rats secreted significantly less endothelin-1 compared with stimulated endothelial cells from HELLP placentas. Neutralization of FasL is associated with decreased MAP and improvement in placental inflammation and endothelial damage in an animal model of HELLP syndrome.
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Flores-Pliego, Arturo, Jael Miranda, Sara Vega-Torreblanca, Yolotzin Valdespino-Vázquez, Cecilia Helguera-Repetto, Aurora Espejel-Nuñez, Héctor Borboa-Olivares, et al. "Molecular Insights into the Thrombotic and Microvascular Injury in Placental Endothelium of Women with Mild or Severe COVID-19." Cells 10, no. 2 (February 10, 2021): 364. http://dx.doi.org/10.3390/cells10020364.
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Clinical manifestations of coronavirus disease 2019 (COVID-19) in pregnant women are diverse, and little is known of the impact of the disease on placental physiology. Severe acute respiratory syndrome coronavirus (SARS-CoV-2) has been detected in the human placenta, and its binding receptor ACE2 is present in a variety of placental cells, including endothelium. Here, we analyze the impact of COVID-19 in placental endothelium, studying by immunofluorescence the expression of von Willebrand factor (vWf), claudin-5, and vascular endothelial (VE) cadherin in the decidua and chorionic villi of placentas from women with mild and severe COVID-19 in comparison to healthy controls. Our results indicate that: (1) vWf expression increases in the endothelium of decidua and chorionic villi of placentas derived from women with COVID-19, being higher in severe cases; (2) Claudin-5 and VE-cadherin expression decrease in the decidua and chorionic villus of placentas from women with severe COVID-19 but not in those with mild disease. Placental histological analysis reveals thrombosis, infarcts, and vascular wall remodeling, confirming the deleterious effect of COVID-19 on placental vessels. Together, these results suggest that placentas from women with COVID-19 have a condition of leaky endothelium and thrombosis, which is sensitive to disease severity.
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Markovic, Stefan, Anne Fages, Tangi Roussel, Ron Hadas, Alexander Brandis, Michal Neeman, and Lucio Frydman. "Placental physiology monitored by hyperpolarized dynamic 13C magnetic resonance." Proceedings of the National Academy of Sciences 115, no. 10 (February 14, 2018): E2429—E2436. http://dx.doi.org/10.1073/pnas.1715175115.
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Placental functions, including transport and metabolism, play essential roles in pregnancy. This study assesses such processes in vivo, from a hyperpolarized MRI perspective. Hyperpolarized urea, bicarbonate, and pyruvate were administered to near-term pregnant rats, and all metabolites displayed distinctive behaviors. Little evidence of placental barrier crossing was observed for bicarbonate, at least within the timescales allowed by 13C relaxation. By contrast, urea was observed to cross the placental barrier, with signatures visible from certain fetal organs including the liver. This was further evidenced by the slower decay times observed for urea in placentas vis-à-vis other maternal compartments and validated by mass spectrometric analyses. A clear placental localization, as well as concurrent generation of hyperpolarized lactate, could also be detected for [1-13C]pyruvate. These metabolites also exhibited longer lifetimes in the placentas than in maternal arteries, consistent with a metabolic activity occurring past the trophoblastic interface. When extended to a model involving the administration of a preeclampsia-causing chemical, hyperpolarized MR revealed changes in urea’s transport, as well as decreases in placental glycolysis vs. the naïve animals. These distinct behaviors highlight the potential of hyperpolarized MR for the early, minimally invasive detection of aberrant placental metabolism.
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Shanes, Elisheva D., Leena B. Mithal, Sebastian Otero, Hooman A. Azad, Emily S. Miller, and Jeffery A. Goldstein. "Placental Pathology in COVID-19." American Journal of Clinical Pathology 154, no. 1 (May 22, 2020): 23–32. http://dx.doi.org/10.1093/ajcp/aqaa089.
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Abstract Objectives To describe histopathologic findings in the placentas of women with coronavirus disease 2019 (COVID-19) during pregnancy. Methods Pregnant women with COVID-19 delivering between March 18, 2020, and May 5, 2020, were identified. Placentas were examined and compared to historical controls and women with placental evaluation for a history of melanoma. Results Sixteen placentas from patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) were examined (15 with live birth in the third trimester, 1 delivered in the second trimester after intrauterine fetal demise). Compared to controls, third trimester placentas were significantly more likely to show at least one feature of maternal vascular malperfusion (MVM), particularly abnormal or injured maternal vessels, and intervillous thrombi. Rates of acute and chronic inflammation were not increased. The placenta from the patient with intrauterine fetal demise showed villous edema and a retroplacental hematoma. Conclusions Relative to controls, COVID-19 placentas show increased prevalence of decidual arteriopathy and other features of MVM, a pattern of placental injury reflecting abnormalities in oxygenation within the intervillous space associated with adverse perinatal outcomes. Only 1 COVID-19 patient was hypertensive despite the association of MVM with hypertensive disorders and preeclampsia. These changes may reflect a systemic inflammatory or hypercoagulable state influencing placental physiology.
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Selvaratnam, Johanna, Haiyan Guan, James Koropatnick, and Kaiping Yang. "Metallothionein-I- and -II-deficient mice display increased susceptibility to cadmium-induced fetal growth restriction." American Journal of Physiology-Endocrinology and Metabolism 305, no. 6 (September 15, 2013): E727—E735. http://dx.doi.org/10.1152/ajpendo.00157.2013.
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Maternal cadmium exposure induces fetal growth restriction (FGR), but the underlying mechanisms remain largely unknown. The placenta is the main organ known to protect the fetus from environmental toxins such as cadmium. In this study, we examine the role of the two key placental factors in cadmium-induced FGR. The first is placental enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which is known to protect the fetus from exposure to high cortisol levels and subsequently FGR, and the second the cadmium binding/sequestering proteins metallotheionein (MT)-I and -II. Using the MT-I/II −/− mouse model, pregnant mice were administered cadmium, following which pups and placentas were collected and examined. MT-I/II−/− pups exposed to cadmium were significantly growth restricted, but neither placental weight nor 11β-HSD2 was altered. Although cadmium administration did not result in any visible structural changes in the placenta, increased apoptosis was detected in MT-I/II−/− placentas following cadmium exposure, with a significant increase in levels of both p53 and caspase 3 proteins. Additionally, glucose transporter (GLUT1) was significantly reduced in MT-I/II−/− placentas of pups exposed to cadmium, whereas zinc transporter (ZnT-1) remained unaltered. Taken together, these results demonstrate that MT-I/II−/− mice are more vulnerable to cadmium-induced FGR. The present data also suggest that increased apoptosis and reduced GLUT1 expression in the placenta contribute to the molecular mechanisms underlying cadmium-induced FGR.
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Tissot van Patot, M. C., J. Bendrick-Peart, V. E. Beckey, N. Serkova, and L. Zwerdlinger. "Greater vascularity, lowered HIF-1/DNA binding, and elevated GSH as markers of adaptation to in vivo chronic hypoxia." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 3 (September 2004): L525—L532. http://dx.doi.org/10.1152/ajplung.00203.2003.
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Vascularity is increased in placentas from high- compared with low-altitude pregnancies. An angiogenic response to hypoxia may protect an organ from further hypoxic insult by increasing blood flow and oxygen delivery to the tissue. We hypothesized that increased placental vascularity is sufficient to adapt to high altitude. Therefore, indexes of hypoxic stress would not be present in placentas from successful high-altitude pregnancies. Full-thickness placental biopsies were 1) collected and frozen in liquid nitrogen within 5 min of placental delivery and 2) fixed in formalin for stereologic analyses at high (3,100 m, n = 10) and low (1,600 m, n = 10) altitude. Hypoxia-inducible transcription factor (HIF-1) activity was analyzed by ELISA. Western blot analyses were used to evaluate HIF-1α, HIF-1β, HIF-2α, von Hippel-Lindau protein, VEGF, Flt-1, enolase, and GAPDH. Magnetic resonance spectroscopy was used to evaluate endogenous metabolism. The ratio of placental capillary surface density to villous surface density was 70% greater at high compared with low altitude. HIF-1 activity and HIF-1-associated proteins were unchanged in placentas from high- vs. low-altitude pregnancies. Placental expression of HIF-1-mediated proteins VEGF, Flt-1, enolase, and GAPDH were unchanged at high vs. low altitude. Succinate, GSH, phosphomonoesters, and ADP were elevated in placenta from high compared with low altitude. Placentas from uncomplicated high-altitude pregnancies have greater vascularity and no indication of significant hypoxic stress at term compared with placentas from low altitude.
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Osifo, E. O., and V. C. Ezeuko. "Histological Assessment of Placental Development Following Intrauterine Exposure to Caffeine in Adult Wistar Rats." Journal of Applied Sciences and Environmental Management 28, no. 4 (April 29, 2024): 1115–20. http://dx.doi.org/10.4314/jasem.v28i4.11.
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In recent years, there have been concerns about human reproductive disorders. Physiological adaptations are crucial for optimal fetal development during pregnancy. The widespread consumption of caffeine by pregnant women raises questions about its impact on maternal physiology and fetal development. Hence, the objective of this study was to evaluate the histological assessment of placenta development following intrauterine exposure to caffeine in adult Wistar rats using appropriate standard techniques. On each gestational day (GD13, GD15, GD17, and GD19), five (5) animals were sampled from each group and their placentas were harvested for histological assessment. The Maternal weight, Fetal Crown Rump Length, Placental weight, Placental diameter major, Placental diameter minor, and fetal weight were taken on the harvested placenta. Results showed varying alterations in the histomorphology of the placenta ranging from delayed differentiation of glycogen cells, dilated and congested blood vessels, vacuolar degeneration of glycogen cell islands, poor development of the labyrinth zone, and dilated fetal capillaries. In conclusion, there is histomorphological evidence that caffeine administration has deleterious effects on the development of the placenta in Wistar rats.
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Schanton, Malena, Julieta L. Maymó, Antonio Pérez-Pérez, Víctor Sánchez-Margalet, and Cecilia L. Varone. "Involvement of leptin in the molecular physiology of the placenta." Reproduction 155, no. 1 (January 2018): R1—R12. http://dx.doi.org/10.1530/rep-17-0512.
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Leptin is a homeostatic regulator in the placenta where it promotes proliferation, protein synthesis and the expression of tolerogenic maternal response molecules such as HLA-G. Leptin also exerts an anti-apoptotic action in placenta controlling the expression of p53 master cell cycle regulator under different stress conditions. On the other hand, leptin is an integrative target of different placental stimuli. The expression of leptin in placenta is regulated by hCG, insulin, steroids, hypoxia and many other growth hormones, suggesting that it might have an important endocrine function in the trophoblastic cells. The leptin expression is induced involving the cAMP/PKA or cAMP/Epac pathways which have profound actions upon human trophoblast function. The activation of PI3K and MAPK pathways also participates in the leptin expression. Estrogens play a central role during pregnancy, particularly 17β-estradiol upregulates the leptin expression in placental cells through genomic and non-genomic actions. The leptin promoter analysis reveals specific elements that are active in placental cells. The transcription factors CREB, AP1, Sp1, NFκB and the coactivator CBP are involved in the placental leptin expression. Moreover, placental leptin promoter is a target of epigenetic marks such as DNA methylation and histone acetylation that regulates not only the leptin expression in placenta during pregnancy but also determines the predisposition of acquiring adult metabolism diseases. Taken together, all these results allow a better understanding of leptin function and regulatory mechanisms of leptin expression in human placental trophoblasts, and support the importance of leptin during pregnancy and in programming adult health.
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Gordon, Zoya, Osnat Eytan, Ariel J. Jaffa, and David Elad. "Hemodynamic analysis of Hyrtl anastomosis in human placenta." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 2 (February 2007): R977—R982. http://dx.doi.org/10.1152/ajpregu.00410.2006.
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The Hyrtl anastomosis is a common connection between the umbilical arteries near the cord insertion in most human placentas. It has been speculated that it equalizes the blood pressure between the territories supplied by the umbilical arteries. However, its functional role in the regulation and distribution of fetal blood flow to the placenta has not yet been explored. A computational model has been developed for quantitative analysis of hemodynamic characteristic of the Hyrtl anastomosis in cases of discordant blood flow in the umbilical arteries. Simulations were performed for cases of either increased placental resistance at the downstream end or reduced arterial blood flow due to some pathologies upstream of one of the arteries. The results indicate that when placental territories of one artery impose increased resistance to fetal blood flow, the Hyrtl anastomosis redistributes the blood flow into the second artery to reduce the large pressure gradients that are developed in the affected artery. When one of the arteries conducts a smaller blood flow into the placenta and a relatively smaller pressure gradient is developed, the Hyrtl anastomosis rebuilds the pressure gradients in the affected artery and redistributes blood flow from the unaffected artery to the affected one to improve placental perfusion. In conclusion, the Hyrtl anastomosis plays the role of either a safety valve or a pressure stabilizer between the umbilical arteries at the placental insertion.
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Panigel, M. "Placental Physiology." Placenta 7, no. 2 (March 1986): 188. http://dx.doi.org/10.1016/s0143-4004(86)80010-8.
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Gardner, Sarah, Jennifer L. Grindstaff, and Polly Campbell. "Placental genotype affects early postpartum maternal behaviour." Royal Society Open Science 6, no. 9 (September 18, 2019): 190732. http://dx.doi.org/10.1098/rsos.190732.
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The mammalian placenta is a source of endocrine signals that prime the onset of maternal care at parturition. While consequences of placental dysfunction for offspring growth are well defined, how altered placental signalling might affect maternal behaviour is unstudied in a natural system. In the cross between sympatric mouse species, Mus musculus domesticus and Mus spretus , hybrid placentas are undersized and show misexpression of genes critical to placental endocrine function. Using this cross, we quantified the effects of placental dysregulation on maternal and anxiety-like behaviours in mice that differed only in pregnancy type. Relative to mothers of conspecific litters, females exposed to hybrid placentas did not differ in anxiety-like behaviours but were slower to retrieve 1-day-old pups and spent less time in the nest on the night following parturition. Early deficits in maternal responsiveness were not explained by reduced ultrasonic vocalization production in hybrid pups and there was no effect of pup genotype on measures of maternal behaviour and physiology collected after the first 24 h postpartum. These results suggest that placental dysregulation leads to poor maternal priming, the effect of which is alleviated by continued exposure to pups. This study provides new insight into the placental mediation of mother–offspring interactions.
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Anthony, Russell V., Amelia R. Tanner, Victoria C. Kennedy, Quinton A. Winger, and Paul J. Rozance. "9 Randel Lecture: In Vivo investigation of pregnancy Physiology." Journal of Animal Science 102, Supplement_1 (March 1, 2024): 52–53. http://dx.doi.org/10.1093/jas/skae019.063.
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Abstract Pregnancy in any mammal requires the integration of three distinct compartments; the maternal, placental and fetal compartments. Compromised function of any of the three compartments can result in suboptimal pregnancy outcomes, including increased morbidity and mortality at delivery, reduced livestock production efficiency and adult-onset of metabolically-related disease in humans. To accurately understand the progression of both normal and compromised pregnancies, therefore, requires the simultaneous assessment of all three compartments, which for most species is not technically feasible. Consequently, over the past 60 yr the pregnant sheep has been used extensively for in vivo investigation of pregnancy physiology. The ability to place indwelling catheters, within both maternal and fetal vessels, allows the simultaneous steady-state assessment of uterine and umbilical blood flows, hormone secretion, and nutrient uptake and utilization of nutrients by each of the three compartments, under non-stressed and non-anesthetized conditions. This has provided unrivalled insight into the physiology of pregnancy, and the realization that the placenta is a highly metabolic tissue, utilizing the majority of oxygen and glucose taken up by the uterus. However, the deficit in studying pregnant sheep is the lack of genetic models, readily available in rodents, that could help define specific gene function during pregnancy. Consequently, we developed in vivo lentiviral-mediated RNA interference (RNAi) methods to specifically alter the abundance of specific gene transcripts/proteins within the placenta, beginning at 9 d of gestation (dGA). Our lentiviral-mediated approach limits the RNAi to the trophectoderm derivatives of the placenta. Initially we used this approach to determine the importance of PRR15 and LIN28 during the establishment of pregnancies, but turned our efforts towards combining in vivo RNAi with steady-state physiological assessments during late gestation to examine the function of genes involved in placental nutrient transport (SLC2A3) and placenta derived hormones (CSH). By creating a placental deficiency in SLC2A3, not only was the fetus smaller and hypoglycemic at mid-gestation, but by interfering with placental glucose uptake, maternal hormone concentrations were also impacted, yet near-term, a distinctly different phenotype was present. For the placental hormone CSH (a.k.a. placental lactogen), CSH RNAi not only impacts placental and fetal growth, but also reductions in uterine blood flow, nutrient fluxes to the fetus, and produces an altered hormonal environment. Combining these methodological approaches provides new and often unexpected insights into the physiological integration of the maternal, placental and fetal compartments. Supported by NIH-NICHD grants HD093701 and HD094952.
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Zhao, Fusheng, Fang Lei, Xiang Yan, Senfeng Zhang, Wen Wang, and Yu Zheng. "Protective Effects of Hydrogen Sulfide Against Cigarette Smoke Exposure-Induced Placental Oxidative Damage by Alleviating Redox Imbalance via Nrf2 Pathway in Rats." Cellular Physiology and Biochemistry 48, no. 5 (2018): 1815–28. http://dx.doi.org/10.1159/000492504.
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Background/Aims: Cigarette smoke exposure (CSE) during pregnancy is a well-recognized health hazard that causes placental damage. Hydrogen sulfide (H2S) has been reported to protect multiple organs from injury. However, the protective effects of H2S have not been tested in the placenta. This study aimed to explore the potential of H2S in protecting placenta against oxidative injury induced by CSE during pregnancy and the possible underlying mechanisms. Methods: Pregnant SD rats were randomly divided into 4 groups: NaCl, NaHS (a donor of H2S), CSE and CSE+NaHS. Placental oxidative damage was detected by 8-hydroxy-2-deoxyguanosine (8-OHdG) stain and malondialdehyde (MDA) assay. Placental redox status was assessed by measuring reactive oxygen species (ROS), total antioxidant capacity (T-AOC) and glutathione (GSH) levels, as well as copper/zinc SOD (SOD1), manganese SOD (SOD2), catalase (CAT) and glutathione peroxidase (GPx) activities and expressions. Meanwhile, nuclear factor erythroid 2-related factor 2 (Nrf2) was analyzed by immunohistochemistry, real-time PCR and Western blot. Results: We found that NaHS markedly reduced the elevated levels of 8-OHdG and MDA induced by CSE. Further, NaHS treatment effectively mitigated CSE-induced placental redox imbalance by inhibiting ROS production, restoring T-AOC level, increasing GSH/GSSG ratio, and augmenting SOD1 SOD2, CAT and GPx activities and expressions. More notably, NaHS administration also reversed the aberrant decrease of Nrf2 due to CSE in rat placentas. Conclusion: Our data demonstrate that H2S can protect against CSE-induced placental oxidative damage probably by alleviating redox imbalance via Nrf2 pathway.
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Wilson, Rebecca L., Weston Troja, Emily K. Sumser, Alec Maupin, Kristin Lampe, and Helen N. Jones. "Insulin-like growth factor 1 signaling in the placenta requires endothelial nitric oxide synthase to support trophoblast function and normal fetal growth." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 320, no. 5 (May 1, 2021): R653—R662. http://dx.doi.org/10.1152/ajpregu.00250.2020.
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Currently, there is no effective treatment for placental dysfunction in utero. In a ligated mouse model of fetal growth restriction (FGR), nanoparticle-mediated human insulin-like 1 growth factor ( hIGF1) gene delivery (NP-Plac1-hIGF1) increased hIGF1 expression and maintained fetal growth. However, whether it can restore fetal growth remains to be determined. Using the endothelial nitric oxide synthase knockout (eNOS−/−) mouse model, a genetic model of FGR, we found that despite inducing expression of hIGF1 in the placentas treated with NP-Plac1-hIGF1 ( P = 0.0425), FGR did not resolve. This was associated with no change to the number of fetal capillaries in the placental labyrinth; an outcome which was increased with NP-Plac1-hIGF1 treatment in the ligated mouse model, despite increased expression of angiopoietin 1 ( P = 0.05), and suggested IGF1 signaling in the placenta requires eNOS to modulate placenta angiogenesis. To further assess this hypothesis, BeWo choriocarcinoma cell line and human placental explant cultures were treated with NP-Plac1-hIGF1, oxidative stress was induced with hydrogen peroxide (H2O2), and NOS activity was inhibited using the inhibitor NG-monomethyl-l-arginine (l-NMMA). In both BeWo cells and explants, the protective effect of NP-Plac1-hIGF1 treatment against H2O2-induced cell death/lactate dehydrogenase release was prevented by eNOS inhibition ( P = 0.003 and P < 0.0001, respectively). This was associated with an increase in mRNA expression of oxidative stress markers hypoxia inducing factor 1α ( HIF1α; P < 0.0001) and ADAM10 ( P = 0.0002) in the NP-Plac1-hIGF1 + H2O2 + l-NMMA-treated BeWo cells. These findings show for the first time the requirement of eNOS/NOS in IGF1 signaling in placenta cells that may have implications for placental angiogenesis and fetal growth.
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Bainbridge, Shannon A., and Graeme N. Smith. "The effect of nicotine on in vitro placental perfusion pressure." Canadian Journal of Physiology and Pharmacology 84, no. 8-9 (September 2006): 953–57. http://dx.doi.org/10.1139/y06-037.
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Cigarette smoking throughout pregnancy is associated with several negative outcomes, of which an increased incidence of intra-uterine growth restriction (IUGR) is most pronounced. Gestationally age-matched infants born to smoking mothers are, on average, 200 g lighter at birth, per pack smoked per day. The mechanisms and specific tobacco compounds responsible for the increased risk of IUGR among smokers have yet to be identified; however, it is widely accepted that smoking women have compromised placental perfusion throughout gestation due to the vasoconstricting effect of nicotine on uterine and placental blood vessels. Despite the universal acceptance of this theory, very little work has been completed to date examining the vasoactive properties of nicotine within the human placenta. The objective of this study was to determine the effect of nicotine on placental vascular function. Normal-term human placentae were obtained after elective cesarean sections. An in vitro placental perfusion system was used; increasing doses of nicotine (20–240 ng/mL) were added to either the maternal (n = 5) or fetal (n = 3) circulation. The basal feto-placental perfusion pressure was 39.87 ± 4.3 mmHg and was not affected by nicotine. This finding supports the hypotheses that nicotine does not directly affect placental microvascular function and that any contribution to fetal growth restriction is likely at the level of placental function (i.e., amino acid transport) and (or) uterine vascular function.
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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 (August 1, 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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Willis, D. M., J. P. O'Grady, J. J. Faber, and K. L. Thornburg. "Diffusion permeability of cyanocobalamin in human placenta." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 250, no. 3 (March 1, 1986): R459—R464. http://dx.doi.org/10.1152/ajpregu.1986.250.3.r459.
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The molecular weight of cyanocobalamin is well suited to distinguish the two patterns of size discrimination found in the hemochorial and epitheliochorial placentas. The concentrations of cyanocobalamin that were used ensured that nondiffusional transport was negligible, and experiments on guinea pigs confirmed that the diffusion permeabilities measured with cyanocobalamin were the same as those expected for inert hydrophilic substances of similar molecular weight. All human studies were performed on volunteers who were scheduled for elective cesarean section under spinal or epidural anesthesia. Endogenous plasma concentrations of cobalamin were measured in 10 pregnant volunteers and their newborns. Ten additional volunteers were given 1 mg of cyanocobalamin by intramuscular injection 44 min before delivery. Placental permeability, calculated as the ratio of fetal uptake and the concentration-time integral between maternal and fetal plasmas, was 14.3 microliter X min-1 X g placental wt-1. The permeability of the human placenta parallels that of the histologically similar guinea pig placenta, at a slightly higher level, up to molecular weights of 1,355.
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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 (December 1, 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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Forstner, Désirée, Jacqueline Guettler, and Martin Gauster. "Changes in Maternal Platelet Physiology during Gestation and Their Interaction with Trophoblasts." International Journal of Molecular Sciences 22, no. 19 (October 3, 2021): 10732. http://dx.doi.org/10.3390/ijms221910732.
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Upon activation, maternal platelets provide a source of proinflammatory mediators in the intervillous space of the placenta. Therefore, platelet-derived factors may interfere with different trophoblast subtypes of the developing human placenta and might cause altered hormone secretion and placental dysfunction later on in pregnancy. Increased platelet activation, and the subsequent occurrence of placental fibrinoid deposition, are linked to placenta pathologies such as preeclampsia. The composition and release of platelet-derived factors change over gestation and provide a potential source of predicting biomarkers for the developing fetus and the mother. This review indicates possible mechanisms of platelet-trophoblast interactions and discusses the effect of increased platelet activation on placenta development.
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Barreto, Rodrigo da Silva Nunes, Ana Claudia Oliveira Carreira, Mônica Duarte da Silva, Leticia Alves Fernandes, Rafaela Rodrigues Ribeiro, Gustavo Henrique Doná Rodrigues Almeida, Bruna Tassia dos Santos Pantoja, Milton Yutaka Nishiyama Junior, and Maria Angelica Miglino. "Mice Placental ECM Components May Provide A Three-Dimensional Placental Microenvironment." Bioengineering 10, no. 1 (December 22, 2022): 16. http://dx.doi.org/10.3390/bioengineering10010016.
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Bioethical limitations impair deeper studies in human placental physiology, then most studies use human term placentas or murine models. To overcome these challenges, new models have been proposed to mimetize the placental three-dimensional microenvironment. The placental extracellular matrix plays an essential role in several processes, being a part of the establishment of materno-fetal interaction. Regarding these aspects, this study aimed to investigate term mice placental ECM components, highlighting its collagenous and non-collagenous content, and proposing a potential three-dimensional model to mimetize the placental microenvironment. For that, 18.5-day-old mice placenta, both control and decellularized (n = 3 per group) were analyzed on Orbitrap Fusion Lumos spectrometer (ThermoScientific) and LFQ intensity generated on MaxQuant software. Proteomic analysis identified 2317 proteins. Using ECM and cell junction-related ontologies, 118 (5.1%) proteins were filtered. Control and decellularized conditions had no significant differential expression on 76 (64.4%) ECM and cell junction-related proteins. Enriched ontologies in the cellular component domain were related to cell junction, collagen and lipoprotein particles, biological process domain, cell adhesion, vasculature, proteolysis, ECM organization, and molecular function. Enriched pathways were clustered in cell adhesion and invasion, and labyrinthine vasculature regulation. These preserved ECM proteins are responsible for tissue stiffness and could support cell anchoring, modeling a three-dimensional structure that may allow placental microenvironment reconstruction.
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SIMCHENKO, A. V., O. A. ALEXEY, and A. A. KUPRASHVILI. "MITOCHONDRIAL DYSFUNCTION IN THE GENESIS OF PLACENTAL PATHOLOGY: PERINATAL OUTCOMES." MODERN PERINATAL MEDICAL TECHNOLOGIES IN SOLVING THE PROBLEM OF DEMOGRAPHIC SECURITY, no. 17 (December 2024): 357–61. https://doi.org/10.63030/2307-4795/2024.17.p.24.
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The human placenta is a unique organ with a temporary functioning period of about 280 days on average. All changes associated with the physiology of mitochondria, the aging process of the placenta, adaptation to changing conditions or dysfunction of the placenta directly affect the performance of the placenta's functions, as well as the development of the fetus. Modern studies studying the causes of intrauterine growth disorders of the fetus demonstrate the implementation of a chain of mechanisms of placental dysfunction, which leads to a slowdown in fetal growth with a subsequent slowdown in physical development at an early age. The literature review presents modern research in the field of studying the adaptive mechanisms of mitochondria during various periods of gestation and their relationship with neonatal pathology
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Hata, Toshiyuki, and Sarah Cajusay-Velasco. "Three-dimensional Power Doppler Ultrasound Study of the Placenta." Donald School Journal of Ultrasound in Obstetrics and Gynecology 8, no. 4 (2014): 400–409. http://dx.doi.org/10.5005/jp-journals-10009-1380.
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ABSTRACT Advanced ultrasound technology has been a valuable tool in the assessment of placental anatomy and physiology. Conventional two-dimensional (2D) sonography reveals placental morphological characteristics, 2D color Doppler can assess blood flow in the placenta, 2D power Doppler can evaluate placental vascular trees, and three-dimensional (3D) ultrasound gives more detailed information on the surface anatomy. Recent advances, such as 3D power Doppler with virtual organ computer aided-analysis (VOCAL) and histogram analysis can measure the placental volume, and assess uteroplacental and fetoplacental perfusions. In particular, ‘placental vascular sonobiopsy’ can specifically evaluate the second- and thirdtrimester placental blood flow and vascularity by obtaining several spherical samples from the placenta that will represent the entire placenta. This article presents normal placental development and pathological findings of the placenta using 3D power Doppler ultrasound, and discusses 3D power Doppler assessments of placental perfusion in high-risk pregnancies, such as fetal growth restriction, pregnancy-induced hypertension and preeclampsia, and, from this basis, re-establishes the importance of 3D power Doppler ultrasound as a screening, diagnostic, and surveillance tool in normal and abnormal pregnancies. How to cite this article Tanaka H, Cajusay-Velasco S, Noguchi J, Hata T. Three-dimensional Power Doppler Ultrasound Study of the Placenta. Donald School J Ultrasound Obstet Gynecol 2014;8(4):400-409.
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Visiedo, Francisco, Fernando Bugatto, Viviana Sánchez, Irene Cózar-Castellano, Jose L. Bartha, and Germán Perdomo. "High glucose levels reduce fatty acid oxidation and increase triglyceride accumulation in human placenta." American Journal of Physiology-Endocrinology and Metabolism 305, no. 2 (July 15, 2013): E205—E212. http://dx.doi.org/10.1152/ajpendo.00032.2013.
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Placentas of women with gestational diabetes mellitus (GDM) exhibit an altered lipid metabolism. The mechanism by which GDM is linked to alterations in placental lipid metabolism remains obscure. We hypothesized that high glucose levels reduce mitochondrial fatty acid oxidation (FAO) and increase triglyceride accumulation in human placenta. To test this hypothesis, we measured FAO, fatty acid esterification, de novo fatty acid synthesis, triglyceride levels, and carnitine palmitoyltransferase activities (CPT) in placental explants of women with GDM or no pregnancy complication. In women with GDM, FAO was reduced by ∼30% without change in mitochondrial content, and triglyceride content was threefold higher than in the control group. Likewise, in placental explants of women with no complications, high glucose levels reduced FAO by ∼20%, and esterification increased linearly with increasing fatty acid concentrations. However, de novo fatty acid synthesis remained unchanged between high and low glucose levels. In addition, high glucose levels increased triglyceride content approximately twofold compared with low glucose levels. Furthermore, etomoxir-mediated inhibition of FAO enhanced esterification capacity by ∼40% and elevated triglyceride content 1.5-fold in placental explants of women, with no complications. Finally, high glucose levels reduced CPT I activity by ∼70% and phosphorylation levels of acetyl-CoA carboxylase by ∼25% in placental explants of women, with no complications. We reveal an unrecognized regulatory mechanism on placental fatty acid metabolism by which high glucose levels reduce mitochondrial FAO through inhibition of CPT I, shifting flux of fatty acids away from oxidation toward the esterification pathway, leading to accumulation of placental triglycerides.
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Schäffer, Leonhard, Johannes Vogel, Christian Breymann, Max Gassmann, and Hugo H. Marti. "Preserved placental oxygenation and development during severe systemic hypoxia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, no. 3 (March 2006): R844—R851. http://dx.doi.org/10.1152/ajpregu.00237.2005.
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Local tissue oxygenation profoundly influences placental development. To elucidate the impact of hypoxia on cellular and molecular adaptation in vivo, pregnant mice at embryonic days 7.5–11.5 were exposed to reduced environmental oxygen (6–7% O2) for various periods of time. Hypoxia-inducible factor (HIF)-1α mRNA was highly expressed in the placenta, whereas HIF-2α was predominantly found in the decidua, indicating that HIF-1 is a relevant oxygen-dependent factor involved in placental development. During severe hypoxia, HIF-1α protein was strongly induced in the periphery but, however, not in the labyrinth layer of the placenta. Accordingly, no indication for tissue hypoxia in this central area was detected with 2-(2-nitro-1 H-imidazol-1-yl)- N-(2,2,3,3,3-pentafluoropropyl)acetamide staining and VEGF expression as hypoxic markers. The absence of significant tissue hypoxia was reflected by preserved placental architecture and trophoblast differentiation. In the search for mechanisms preventing local hypoxia, we found upregulation of endothelial nitric oxide synthase (NOS) expression in the labyrinth layer. Inhibition of NOS activity by Nω-nitro-l-arginine methyl ester application resulted in ubiquitous placental tissue hypoxia. Our results show that placental oxygenation is preserved even during severe systemic hypoxia and imply that NOS-mediated mechanisms are involved to protect the placenta from maternal hypoxia.
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Magnusson-Olsson, Anne Liese, Susanne Lager, Bo Jacobsson, Thomas Jansson, and Theresa L. Powell. "Effect of maternal triglycerides and free fatty acids on placental LPL in cultured primary trophoblast cells and in a case of maternal LPL deficiency." American Journal of Physiology-Endocrinology and Metabolism 293, no. 1 (July 2007): E24—E30. http://dx.doi.org/10.1152/ajpendo.00571.2006.
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Maternal hypertriglyceridemia is a normal condition in late gestation and is an adaptation to ensure an adequate nutrient supply to the fetus. Placental lipoprotein lipase (LPL) is involved in the initial step in transplacental fatty acid transport as it hydrolyzes maternal triglycerides (TG) to release free fatty acids (FFA). We investigated LPL activity and protein (Western blot) and mRNA expression (real-time RT-PCR) in the placenta of an LPL-deficient mother with marked hypertriglyceridemia. The LPL activity was fourfold lower, LPL protein expression 50% lower, and mRNA expression threefold higher than that of normal, healthy placentas at term ( n = 4–7). To further investigate the role of maternal lipids in placental LPL regulation, we isolated placental cytotrophoblasts from term placentas and studied LPL activity and protein and mRNA expression after incubation in Intralipid (as a source of TG) and oleic, linoleic, and a combination of oleic, linoleic, and arachidonic acids as well as insulin. Intralipid (40 and 400 mg/dl) decreased LPL activity by ≈30% ( n = 10–14, P < 0.05) and 400 μM linoleic and linoleic-oleic-arachidonic acid ( n = 10) decreased LPL activity by 37 and 34%, respectively. No major changes were observed in LPL protein or mRNA expression. We found no effect of insulin on LPL activity or protein expression in the cultured trophoblasts. To conclude, the activity of placental LPL is reduced by high levels of maternal TG and/or FFA. This regulatory mechanism may serve to counteract an excessive delivery of FFA to the fetus in conditions where maternal TG levels are markedly increased.
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Paterson, P. G., B. Sarkar, and S. H. Zlotkin. "The effect of zinc levels in fetal circulation on zinc clearance across the in situ perfused guinea pig placenta." Canadian Journal of Physiology and Pharmacology 68, no. 11 (November 1, 1990): 1401–6. http://dx.doi.org/10.1139/y90-213.
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Although zinc is essential for normal fetal growth and development, little is known about factors that influence its transfer across the placenta. The in situ perfused guinea pig placenta model was used to study the influence of the zinc concentration of fetal circulation on maternofetal placental zinc transfer. A placenta of the anaesthetized sow was perfused (on the fetal side) with a physiological perfusate via the umbilical vessels, with the fetus excluded. The sow was infused intravenously with 65zinc as a tracer of placental Zn clearance, and with antipyrine as an indirect indicator of maternal placental blood flow. Maternal plasma and placental effluent samples collected at intervals were counted for 65zinc by gamma counter, and the absorbance of nitrosated antipyrine was measured at 350 nm. Varying the mean zinc concentration in the perfusate from 0.176 to 1.87 mg/L had no effect on relative zinc clearance calculated as zinc clearance/antipyrine clearance (mean ± SEM; 0.085 ± 0.010 vs. 0.114 ± 0.018; n = 6; p > 0.05). The results suggest that short-term changes in fetal zinc status do not influence placental zinc transfer.Key words: placenta, zinc, transport, trophoblast.
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de Vrijer, Barbra, Timothy R. H. Regnault, Randall B. Wilkening, Giacomo Meschia, and Frederick C. Battaglia. "Placental uptake and transport of ACP, a neutral nonmetabolizable amino acid, in an ovine model of fetal growth restriction." American Journal of Physiology-Endocrinology and Metabolism 287, no. 6 (December 2004): E1114—E1124. http://dx.doi.org/10.1152/ajpendo.00259.2004.
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Reductions in fetal plasma concentrations of certain amino acids and reduced amino acid transport in vesicle studies suggest impaired placental amino acid transport in human fetal growth restriction (FGR). In the present study, we tested the hypothesis of an impairment in amino acid transport in the ovine model of hyperthermia-induced FGR by determining transplacental and placental retention and total placental clearance of a branched-chain amino acid (BCAA) analog, the nonmetabolizable neutral amino acid aminocyclopentane-1-carboxylic acid (ACP), in singleton control (C) and FGR pregnancies at 135 days gestation age (dGA; term 147 dGA). At study, based on the severity of the placental dysfunction, FGR fetuses were allocated to severe (sFGR, n = 6) and moderate FGR (mFGR, n = 4) groups. Fetal (C, 3,801.91 ± 156.83; mFGR, 2,911.33 ± 181.35; sFGR, 1,795.99 ± 238.85 g; P < 0.05) and placental weights (C, 414.38 ± 38.35; mFGR, 306.23 ± 32.41; sFGR, 165.64 ± 28.25 g; P < 0.05) were reduced. Transplacental and total placental clearances of ACP per 100 g placenta were significantly reduced in the sFGR but not in the mFGR group, whereas placental retention clearances were unaltered. These data indicate that both entry of ACP into the placenta and movement from the placenta into fetal circulation are impaired in severe ovine FGR and support the hypothesis of impaired placental BCAA transport in severe human FGR.
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Mathias, Anita A., Jane Hitti, and Jashvant D. Unadkat. "P-glycoprotein and breast cancer resistance protein expression in human placentae of various gestational ages." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 4 (October 2005): R963—R969. http://dx.doi.org/10.1152/ajpregu.00173.2005.
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Placental efflux transporters such as P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) protect the developing fetus from exposure to potentially toxic xenobiotics. However, little is known about the expression of these transporters in human placentae of different gestational ages. Therefore, we quantified the expression of P-gp and BCRP in human placentae of different gestational ages. We also measured the expression of various nuclear regulatory factors such as the pregnane xenobiotic factor to determine whether their expression also changes with gestational age. Syncitial microvillous plasma membranes were isolated from human placentae of various gestational ages (60–90 days, 90–120 days, and full-term C-section placentae). P-gp and BCRP expression (protein) in these preparations were measured by Western blot analysis followed by an ELISA. Expression (mRNA) of P-gp, BCRP, and nuclear regulatory factors in the placentae were quantified by quantitative real-time PCR. P-gp expression (relative to that of alkaline phosphatase) was significantly ( P < 0.05) higher (44.8-fold as protein; 6.5-fold as mRNA) in early gestational age human placentae (60–90 days) vs. term placentae. In contrast, BCRP (protein and mRNA) and nuclear regulatory factors (mRNA) expression in placental tissue did not change significantly with gestational age. However, placental expression of P-gp and human chorionic gonadotropin-β (hCG-β) transcripts was highly correlated ( r = 0.73; P < 0.0001; Spearman rank correlation). Expression of P-gp, but not BCRP, decreases dramatically with gestational age in human placentae. This decrease in P-gp expression is not caused by a change in expression of nuclear receptor transcripts but appears to be related to hCG-β expression. The placental P-gp expression appears to be upregulated in early pregnancy to protect the fetus from xenobiotic toxicity at a time when it is most vulnerable to such toxicity.
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Mandò, C., C. De Palma, T. Stampalija, G. M. Anelli, M. Figus, C. Novielli, F. Parisi, E. Clementi, E. Ferrazzi, and I. Cetin. "Placental mitochondrial content and function in intrauterine growth restriction and preeclampsia." American Journal of Physiology-Endocrinology and Metabolism 306, no. 4 (February 15, 2014): E404—E413. http://dx.doi.org/10.1152/ajpendo.00426.2013.
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Intrauterine growth restriction (IUGR) and pregnancy hypertensive disorders such as preeclampsia (PE) associated with IUGR share a common placental phenotype called “placental insufficiency”, originating in early gestation when high availability of energy is required. Here, we assess mitochondrial content and the expression and activity of respiratory chain complexes (RCC) in placental cells of these pathologies. We measured mitochondrial (mt)DNA and nuclear respiratory factor 1 ( NRF1) expression in placental tissue and cytotrophoblast cells, gene and protein expressions of RCC (real-time PCR and Western blotting) and their oxygen consumption, using the innovative technique of high-resolution respirometry. We analyzed eight IUGR, six PE, and eight uncomplicated human pregnancies delivered by elective cesarean section. We found lower mRNA levels of complex II, III, and IV in IUGR cytotrophoblast cells but no differences at the protein level, suggesting a posttranscriptional compensatory regulation. mtDNA was increased in IUGR placentas. Both mtDNA and NRF1 expression were instead significantly lower in their isolated cytotrophoblast cells. Finally, cytotrophoblast RCC activity was significantly increased in placentas of IUGR fetuses. No significant differences were found in PE placentas. This study provides genuine new data into the complex physiology of placental oxygenation in IUGR fetuses. The higher mitochondrial content in IUGR placental tissue is reversed in cytotrophoblast cells, which instead present higher mitochondrial functionality. This suggests different mitochondrial content and activity depending on the placental cell lineage. Increased placental oxygen consumption might represent a limiting step in fetal growth restriction, preventing adequate oxygen delivery to the fetus.
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Castillo-Castrejon, Marisol, Thomas Jansson, and Theresa L. Powell. "No evidence of attenuation of placental insulin-stimulated Akt phosphorylation and amino acid transport in maternal obesity and gestational diabetes mellitus." American Journal of Physiology-Endocrinology and Metabolism 317, no. 6 (December 1, 2019): E1037—E1049. http://dx.doi.org/10.1152/ajpendo.00196.2019.
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Pregnancies complicated by obesity and/or gestational diabetes (GDM) are associated with peripheral insulin resistance; however, the insulin responsiveness of the placenta in these pregnancy complications remains largely unknown. We tested the hypothesis that primary human trophoblast cells and placental villous explants will be insulin responsive, characterized by amino acid transport, Akt and Erk activity with maternal obesity, and/or GDM. We evaluated term placentas from women with normal body mass index (BMI) (normal; n = 15), obesity (OB; n = 11), normal BMI with GDM (N-GDM; n = 11), and obesity with GDM (OB-GDM; n = 11). In a subgroup, primary human trophoblast cells (PHT) were isolated, and in an independent subgroup placental villous explants were exposed to varying concentrations of insulin. Amino acid transport capacity and insulin signaling activity were determined. Insulin significantly increased amino acid transport activity to a similar degree in PHT cells isolated from normal (+21%), N-GDM (+38%), OB (+37%), and OB-GDM (+35%) pregnancies. Insulin increased Akt and Erk phosphorylation in PHT cells (3-fold) and in villous explants (2-fold) in all groups to a similar degree. In contrast to the peripheral maternal insulin resistance commonly associated with obesity and/or GDM, we found that the placenta is insulin sensitive in these pregnancy complications. We suggest that elevated maternal insulin levels in pregnancies complicated by obesity and/or GDM promote critical placental functions, including amino acid transport. Insulin-stimulated placental nutrient delivery may contribute to the increased risk of fetal overgrowth and adiposity in these pregnancies. Moreover, our findings may inform efforts to optimize insulin regimens for women with GDM.
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do Imperio, Guinever Eustaquio, Enrrico Bloise, Mohsen Javam, Phetcharawan Lye, Andrea Constantinof, Caroline Dunk, Fernando Marcos dos Reis, et al. "Chorioamnionitis Induces a Specific Signature of Placental ABC Transporters Associated with an Increase of miR-331-5p in the Human Preterm Placenta." Cellular Physiology and Biochemistry 45, no. 2 (2018): 591–604. http://dx.doi.org/10.1159/000487100.
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Background/Aims: The ATP-binding cassette (ABC) transporters mediate drug biodisposition and immunological responses in the placental barrier. In vitro infective challenges alter expression of specific placental ABC transporters. We hypothesized that chorioamnionitis induces a distinct pattern of ABC transporter expression. Methods: Gene expression of 50 ABC transporters was assessed using TaqMan® Human ABC Transporter Array, in preterm human placentas without (PTD; n=6) or with histological chorioamnionitis (PTDC; n=6). Validation was performed using qPCR, immunohistochemistry and Western blot. MicroRNAs known to regulate P-glycoprotein (P-gp) were examined by qPCR. Results: Up-regulation of ABCB9, ABCC2 and ABCF2 mRNA was detected in chorioamnionitis (p<0.05), whereas placental ABCB1 (P-gp; p=0.051) and ABCG2 (breast cancer resistance protein-BCRP) mRNA levels (p=0.055) approached near significant up-regulation. In most cases, the magnitude of the effect significantly correlated to the severity of inflammation. Upon validation, increased placental ABCB1 and ABCG2 mRNA levels (p<0.05) were observed. At the level of immunohistochemistry, while BCRP was increased (p<0.05), P-gp staining intensity was significantly decreased (p<0.05) in PTDC. miR-331-5p, involved in P-gp suppression, was upregulated in PTDC (p<0.01) and correlated to the grade of chorioamnionitis (p<0.01). Conclusions: Alterations in the expression of ABC transporters will likely lead to modified transport of clinically relevant compounds at the inflamed placenta. A better understanding of the potential role of these transporters in the events surrounding PTD may also enable new strategies to be developed for prevention and treatment of PTD.
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Das, Utpala G., Jing He, Richard A. Ehrhardt, William W. Hay, and Sherin U. Devaskar. "Time-dependent physiological regulation of ovine placental GLUT-3 glucose transporter protein." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 6 (December 1, 2000): R2252—R2261. http://dx.doi.org/10.1152/ajpregu.2000.279.6.r2252.
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We immunolocalized the GLUT-3 glucose transporter isoform versus GLUT-1 in the late-gestation epitheliochorial ovine placenta, and we examined the effect of chronic maternal hyperglycemia and hypoglycemia on placental GLUT-3 concentrations. GLUT-3 was limited to the apical surface of the trophoectoderm, whereas GLUT-1 was on the basolateral and apical surfaces of this cell layer and in the epithelial cells lining the placental uterine glands. GLUT-3 concentrations declined at 17–20 days of chronic hyperglycemia ( P < 0.05), associated with increased uterine and uteroplacental net glucose uptake rate, but a normal fetal glucose uptake rate was observed. Chronic hypoglycemia did not change GLUT-3 concentrations, although uterine, uteroplacental, and fetal net glucose uptake rates were decreased. Thus maternal hyperglycemia causes a time-dependent decline in the entire placental glucose transporter pool (GLUT-1 and GLUT-3). In contrast, maternal hypoglycemia decreases GLUT-1 but not GLUT-3, resulting in a relatively increased GLUT-3 contribution to the placental glucose transporter pool, which could maintain glucose delivery to the placenta relative to the fetus when maternal glucose is low.
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Soliman, Natasha. "HOW IT WORKS 5: PHYSIOLOGICAL BIRTH OF THE PLACENTA." Practising Midwife 27, no. 02 (March 1, 2024): 12–15. http://dx.doi.org/10.55975/nuap7898.
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In this article I talk about physiological birth of the placenta by exploring the anatomy and physiology of the placenta and its role in childbirth, pairing this with the skills required to facilitate a physiological placental birth. It is important for midwives to understand the anatomy and physiology behind the skill set required to provide care during physiological birth of the placenta and to understand how midwifery practice can influence achieving this for women and birthing people.
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Sidle, Elizabeth H., Richard Casselman, and Graeme N. Smith. "Effect of cigarette smoke on placental antioxidant enzyme expression." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 2 (August 2007): R754—R758. http://dx.doi.org/10.1152/ajpregu.00505.2006.
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Cigarette smoking is associated with systemic oxidative stress leading to an upregulation of antioxidant systems [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and heme oxygenase (HO)] in some tissues, but the response in the human placenta is unknown. The aim of this study was to determine the effect of cigarette smoke exposure on placental antioxidant expression in vivo, as well as the effect on antioxidant expression in the human trophoblast choriocarcinoma (HTR)-8SVNeo cell line. In the in vivo experiment, normal-term placentas were obtained following elective caesarean section. The chorionic villi (CV), anchoring villi (AV), and basal plate (BP) were dissected, and Western blot analysis was carried out for HO-1, HO-2, SOD, CAT, and GPx. In vitro experiment, a cigarette smoke extract (CSE) was prepared by bubbling the smoke form three cigarettes through 15 ml of RPMI. This 100% CSE was syringe filtered and diluted to 0.1, 0.5, 1, 2, 5, and 10% concentrations. HTR-8SVNeo cells were cultured with the CSE for 48 h. The cells were harvested, protein was extracted, and run on SDS-PAGE gels, and Western blot analysis was carried out for HO-1, HO-2, SOD, and CAT. Immunofluorescence for HTR-8SVNeo cells HO-1 was carried out following increasing concentrations of CSE. In the in vivo experiment, HO-1 and HO-2 expression was increased in the BP of placentas from smokers compared with nonsmokers. CAT, GPx, and SOD levels in all placental regions, as well as HO-1 and HO-2 expression in the AV and CV were unchanged. In the in vitro experiment, The 5%, 10%, and 20% dilutions were toxic to the cells. The 0.1% CSE solution did not significantly alter HO-1 expression. Treatment with the 0.5%, 1% and 2% CSE solutions resulted in a dose-dependent increase in HO-1 expression. None of the CSE treatments resulted in a significant alteration in HO-2, SOD, GPx, or CAT expression. HO-1 immunoflourescence confirmed the HO-1 expression studies. Cigarette smoke exposure increases HO-1 and HO-2 expression in the placental basal plate and increases HO-1 expression in the HTR-8SVNeo cell line. Increased HO-1 and HO-2 protein expression may increase the production of the antioxidants biliverdin and bilirubin, which are products of heme metabolism. This could function to reduce the oxidative load that is released into the maternal plasma from the preeclamptic placenta and may contribute to the observed decreased incidence of preeclampsia in smokers.
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Mandò, Chiara, Valeria M. Savasi, Gaia M. Anelli, Silvia Corti, Anaïs Serati, Fabrizia Lisso, Chiara Tasca, Chiara Novielli, and Irene Cetin. "Mitochondrial and Oxidative Unbalance in Placentas from Mothers with SARS-CoV-2 Infection." Antioxidants 10, no. 10 (September 24, 2021): 1517. http://dx.doi.org/10.3390/antiox10101517.
Full textAbstract:
SARS-CoV-2 infection has been related to adverse pregnancy outcomes. A placental role in protecting the fetus from SARS-CoV-2 infection has been documented. Nevertheless, it is still unclear how the placenta is affected in SARS-CoV-2 infection. Here we assessed placental mitochondrial (mt) and oxidative features in COVID-19 and healthy mothers. mtDNA levels, DNA oxidative damage, expression levels of genes involved in antioxidant defenses, mitochondrial dynamics and respiratory chain subunits were investigated in placentas from singleton pregnancies of 30 women with SARS-CoV-2 infection during the third trimester (12 asymptomatic, 18 symptomatic) and 16 controls. mtDNA levels decreased in COVID-19 placentas vs. controls and inversely correlated with DNA oxidative damage, which increased in the symptomatic group. Antioxidant gene expressions decreased in SARS-CoV-2 mothers (CAT, GSS). Symptomatic cases also showed a lower expression of respiratory chain (NDUFA9, SDHA, COX4I1) and mt dynamics (DNM1L, FIS1) genes. Alterations in placental mitochondrial features and oxidative balance in COVID-19-affected mothers might be due to the impaired intrauterine environment, generated by systemic viral effects, leading to a negative vicious circle that worsens placental oxidative stress and mitochondrial efficiency. This likely causes cell homeostasis dysregulations, raising the potential of possible long-term effects.
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Corrêa, Isis Paloppi, Rodrigo Ruano, Nilton Hideto Takiuti, Rossana Pulcinelli Vieira Francisco, Estela Bevilacqua, and Marcelo Zugaib. "Expression of angiogenic factors in placenta of stressed rats." Reproduction, Fertility and Development 24, no. 6 (2012): 851. http://dx.doi.org/10.1071/rd11202.
Full textAbstract:
The aim of the present study was to analyse the influence of stress on pregnant rats, particularly in terms of maternal, placental and fetal weight, placental morphology and placental gene expression of the angiogenic factors Vegfa and Pgf and their receptors. The parameters were evaluated on gestation Day 20. Maternal, fetal and placental weights were statistically lower in stressed animals than controls, suggesting abnormalities in gestational physiology. Morphologically the placentas of rats subjected to stress were reduced in size and weight, with few glycogen cells and a significant increase in the number of apoptotic cells. Stress caused an increase in placental gene expression of Vegfa (P < 0.05) and a reduction in Pgf, Flt1 and Kdr expression (P < 0.05). It has been suggested that increased VEGF is associated with vasodilatation and hypotension, but in this model persistent hypertension was present. This study suggests that the limited hypotensive Vegfa response to stress-induced hypertension could result from reduced expression of Flt1/Kdr disrupting specific VEGF pathways. These findings may elucidate one of the multiple possible factors underlying how stress modulates placental physiology, and could aid the understanding of stress-induced gestational disorders.
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Angioni, S., G. Botticelli, M. C. Galassi, A. D. Genazzani, A. C. Mancini, F. Amato, F. Petraglia, and A. R. Genazzani. "Cytokines in placental physiology." Advances in Neuroimmunology 1, no. 2 (May 1991): 180–84. http://dx.doi.org/10.1016/s0960-5428(06)80222-6.
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Lazo-de-la-Vega-Monroy, Maria-Luisa, Karen-Alejandra Mata-Tapia, Juan-Antonio Garcia-Santillan, Maria-Angelica Corona-Figueroa, Martha-Isabel Gonzalez-Dominguez, Hector-Manuel Gomez-Zapata, Juan-Manuel Malacara, Leonel Daza-Benitez, and Gloria Barbosa-Sabanero. "Association of placental nutrient sensing pathways with birth weight." Reproduction 160, no. 3 (September 2020): 455–68. http://dx.doi.org/10.1530/rep-20-0186.
Full textAbstract:
Birth weight (BW) is an important indicator for newborn health. Both high and low BW is associated with increased risks for adult metabolic diseases. AMPK (AMP-activated protein kinase), mTOR (mechanistic target of rapamycin), and insulin/IGF1 (insulin-like growth factor 1) pathways may function as placental sensors of maternal hormonal and nutritional status. However, the physiological role of these pathways in placenta has not been completely elucidated. To evaluate expression and activation of AMPK, mTOR, and insulin/IGF1 pathways and its association with placental weight (PW), BW, and maternal hormonal and metabolic status, we performed a cross-sectional study in placentas from non-obese mothers with SGA (n = 17), AGA (n = 19) and LGA (n = 10) newborns. We analyzed placental expression of total and phosphorylated key proteins from the AMPK, mTOR and insulin/IGF1 pathways. Maternal and cord blood hormones were determined by ELISA. AMPK and LKB1 activation correlated negatively with PW and BW, cord leptin, and pregestational BMI. Placental SIRT1 inversely correlated with BW, cord leptin, neonatal HOMA-IR, and maternal IGF1. PGC1α correlated negatively with PW and BW. Phosphorylated mTOR positively correlated with maternal glucose, PW and BW. IGF1R was lower in SGA. No changes in p-IGF1R, INSRb, total AKT or p-AKT were found, and pPDK1 was lower in SGA and LGA. These results suggest that placental AMPK, insulin/IGF1, and mTOR pathways may influence fetal growth, perhaps regulating placental physiology, even in metabolically healthy pregnancies. Our study highlights these nutrient sensing pathways as potential molecular mechanisms modulating placental adaptations and, thus, long-term metabolic health.
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Roos, S., T. L. Powell, and T. Jansson. "Human placental taurine transporter in uncomplicated and IUGR pregnancies: cellular localization, protein expression, and regulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 4 (October 2004): R886—R893. http://dx.doi.org/10.1152/ajpregu.00232.2004.
Full textAbstract:
Transplacental transfer is the fetus' primary source of taurine, an essential amino acid during fetal life. In intrauterine growth restriction (IUGR), placental transport capacity of taurine is reduced and fetal taurine levels are decreased. We characterized the protein expression of the taurine transporter (TAUT) in human placenta using immunocytochemistry and Western blotting, tested the hypothesis that placental protein expression of TAUT is reduced in IUGR, and investigated TAUT regulation by measuring the Na+-dependent taurine uptake in primary villous fragments after 1 h of incubation with different effectors. TAUT was primarily localized in the syncytiotrophoblast microvillous plasma membrane (MVM). TAUT was detected as a single 70-kDa band, and MVM TAUT expression was unaltered in IUGR. The PKC activator PMA and the nitric oxide (NO) donor 3-morpholinosydnonimine decreased TAUT activity ( P < 0.05, n = 7–15). However, none of the tested hormones, e.g., leptin and growth hormone, altered TAUT activity significantly. PKC activity measured in MVM from control and IUGR placentas was not different. In conclusion, syncytiotrophoblast TAUT is strongly polarized to the maternal-facing plasma membrane. MVM TAUT expression is unaltered in IUGR, suggesting that the reduced MVM taurine transport in IUGR is due to changes in transporter activity. NO release downregulates placental TAUT activity, and it has previously been shown that IUGR is associated with increased fetoplacental NO levels. NO may therefore play an important role in downregulating MVM TAUT activity in IUGR.
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Greupink, Rick. "1 Placental pharmacology studies to characterize the effects and disposition of pharmaceuticals: lessons from human tissues and cells for improving drug safety in pregnancy." Archives of Disease in Childhood 108, no. 6 (May 18, 2023): A1.1—A1. http://dx.doi.org/10.1136/archdischild-2023-esdppp.1.
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The placenta plays a key role in maintaining a healthy pregnancy. In order to improve drug safety during pregnancy, it is therefore relevant to understand to which extent and at which rate drugs are transferred across the placenta and how pharmaceuticals may affect placental function. Translational and predictive pharmacology studies based on human tissues and cells are becoming increasingly important in characterizing the effects and disposition of pharmaceuticals. With regard to the placenta, such approaches may for example be readily combined with physiology-based pharmacokinetic (PBPK) modeling to predict fetal exposure of drugs, as well as placental tissue exposure in the clinic. In addition, placental tissue and cells can be used to study potential effects of drugs, as well. The current presentation, will highlight several studies that investigated the placental disposition and effects of both small and large molecule pharmaceuticals, as well as how such data can help to better understand the clinical pharmacology of therapeutics.
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Nakamura, Hiroyuki, Hirofumi Nagase, Masami Yoshida, Keiki Ogino, Toshio Seto, Kotaro Hatta, and Ichiyo Matsuzaki. "Opioid peptides mediate heat stress-induced immunosuppression during pregnancy." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 3 (March 1, 1998): R672—R676. http://dx.doi.org/10.1152/ajpregu.1998.274.3.r672.
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To clarify the involvement of the opioid system in enhanced immunosuppression induced by heat stress during pregnancy, we examined the effects of heat exposure and intraperitoneal administration of opioid receptor antagonist naloxone on β-endorphin (β-EP) in blood, pituitary lobes, and placenta as well as splenic natural killer cell activity (NKCA) and placental steroids in pregnant rats at 15–16 days gestation. Two-way analysis of variance revealed significant increases in blood β-EP induced by heat and naloxone and a significant interaction between heat and naloxone on blood β-EP and progesterone (P). Whereas heat reduced NKCA, intraperitoneal administration of naloxone reversed it. Significant increases in blood and placental β-EP induced by both heat and naloxone administration and a significant interaction on blood and placental β-EP was observed. These results suggest that immunosuppression produced by heat stress during pregnancy is mediated by the opioid system. A positive correlation between β-EP in blood and placenta during heat and naloxone administration suggests that increased placental β-EP during heat results in hypersecretion of β-EP into blood. P increased by heat during pregnancy may be involved in the immunosuppression.
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Borke, James L., Ariel Caride, Anil K. Verma, Lucky K. Kelley, Carl H. Smith, John T. Penniston, and Rajiv Kumar. "Calcium pump epitopes in placental trophoblast basal plasma membranes." American Journal of Physiology-Cell Physiology 257, no. 2 (August 1, 1989): C341—C346. http://dx.doi.org/10.1152/ajpcell.1989.257.2.c341.
Full textAbstract:
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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Watson, Erica D., and James C. Cross. "Development of Structures and Transport Functions in the Mouse Placenta." Physiology 20, no. 3 (June 2005): 180–93. http://dx.doi.org/10.1152/physiol.00001.2005.
Full textAbstract:
The placenta is essential for sustaining the growth of the fetus during gestation, and defects in its function result in fetal growth restriction or, if more severe, fetal death. Several molecular pathways have been identified that are essential for development of the placenta, and mouse mutants offer new insights into the cell biology of placental development and physiology of nutrient transport.
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John, Rosalind M. "Epigenetic regulation of placental endocrine lineages and complications of pregnancy." Biochemical Society Transactions 41, no. 3 (May 23, 2013): 701–9. http://dx.doi.org/10.1042/bst20130002.
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A defining feature of mammals is the development in utero of the fetus supported by the constant flow of nutrients from the mother obtained via a specialized organ: the placenta. The placenta is also a major endocrine organ that synthesizes vast quantities of hormones and cytokines to instruct both maternal and fetal physiology. Nearly 20 years ago, David Haig and colleagues proposed that placental hormones were likely targets of the epigenetic process of genomic imprinting in response to the genetic conflicts imposed by in utero development [Haig (1993) Q. Rev. Biol. 68, 495–532]. There are two simple mechanisms through which genomic imprinting could regulate placental hormones. First, imprints could directly switch on or off alleles of specific genes. Secondly, imprinted genes could alter the expression of placental hormones by regulating the development of placental endocrine lineages. In mice, the placental hormones are synthesized in the trophoblast giant cells and spongiotrophoblast cells of the mature placenta. In the present article, I review the functional role of imprinted genes in regulating these endocrine lineages, which lends support to Haig's original hypothesis. I also discuss how imprinting defects in the placenta may adversely affect the health of the fetus and its mother during pregnancy and beyond.
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Kennedy, L. A., S. Mukerji, and M. J. Elliott. "The ontogeny of placental Na+–K+ ATPase in the mouse and its impairment by ethanol." Canadian Journal of Physiology and Pharmacology 64, no. 7 (July 1, 1986): 1032–37. http://dx.doi.org/10.1139/y86-176.
Full textAbstract:
We have investigated the normal ontogeny of Na+–K+ ATPase in the mouse placenta and the possibility that impairment in placental transport capacity, as reflected in reductions in NA+–K+ ATPase activity, is associated with alcohol-related embryonic growth restriction. We have demonstrated that over the normal course of pregnancy there is a dramatic increase in placental NA+–K+ ATPase activity which occurs in concert with the embryofetal body growth spurt. Maternal ethanol administration during the early period of placental enzymogenesis (days 7–9) resulted in a significant reduction (up to 40%) of placental Na+–K+ ATPase activity on day 15. Both the severity and the frequency of the reduction were dose dependent. The effect was associated with significant reductions in embryonic body and brain weight but no change in body length or prenatal mortality. Incubation of term placental fragments for 2 h in increasing concentrations of ethanol resulted in a comparable reduction in enzyme activity. Our studies demonstrate that direct ethanol exposure produces a reduction of placental Na+–K+ ATPase activity, that exposure during the early stages of enzymogenesis results in persistent reductions in Na+–K+ ATPase activity in the mature placenta, and that this effect is associated with deficits of embryonic body and brain growth. A direct causal relationship has not been proven; however, it is conceivable that the correlation between reduced placental Na+–K+ ATPase activity and impaired embryofetal growth reflects a common causal pathway.
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Drynda, Robert, Shanta J. Persaud, James E. Bowe, and Peter M. Jones. "The Placental Secretome: Identifying Potential Cross-Talk Between Placenta and Islet β-Cells." Cellular Physiology and Biochemistry 45, no. 3 (2018): 1165–71. http://dx.doi.org/10.1159/000487357.
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Background/Aims: Insulin-secreting islet β-cells adapt to the insulin resistance associated with pregnancy by increasing functional β-cell mass, but the placental signals involved in this process are not well defined. In the current study, we analysed expression of G-protein coupled receptor (GPCR) mRNAs in mouse islets and islet GPCR ligand mRNAs in placenta during pregnancy to generate an atlas of potential interactions between the placenta and β-cells to inform future functional studies of islet adaptive responses to pregnancy. Methods: Quantative RT-PCR arrays were used to measure mRNA expression levels of: (i) 342 GPCRs in islets from non-pregnant mice, and in islets isolated from mice on gestational days 12 and 18; (ii) 126 islet GPCR ligands in mouse placenta at gestational days 12 and 18. Results: At gestational day 12, a time of rapid expansion of the β-cell mass, 189 islet GPCR mRNAs were quantifiable, while 79 of the 126 known islet GPCR ligand mRNAs were detectable in placental extracts. Approximately half of the quantifiable placental GPCR ligand genes were of unknown function in β-cells. The expression of some islet GPCR and placental ligand mRNAs varied during pregnancy, with altered expression of both GPCR and ligand mRNAs by gestational day 18. Conclusion: The current study has revealed numerous potential routes for interaction between the placenta and islets, and offers an atlas to inform further functional studies of their roles in adaptive responses to pregnancy, and in the regulation of the β-cell mass.