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Journal articles on the topic 'Physiologie placentaire'
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1
Schaaps, Jean-Pierre, Henri Thoumsin, Jean-Michel Foidart, and Jean Hustin. "Physiologie placentaire." EMC - Obstétrique 21, no. 4 (1998): 1–20. https://doi.org/10.1016/s0246-0335(19)30293-5.
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Deloison, B., A. E. Millischer, and L. J. Salomon. "IRM placentaire : physiologie et pathologie." Gynécologie Obstétrique & Fertilité 41, no. 6 (June 2013): 394–403. http://dx.doi.org/10.1016/j.gyobfe.2013.04.004.
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FRANKENNE, F., G. PIRENS, F. GOMEZ, and G. HENNEN. "Découverte d'un variant placentaire de l'hormone de croissance humaine : biochimie, physiologie et implication dans la sécrétion des formes hypophysaires." Reproduction Nutrition Développement 27, no. 2B (1987): 523–24. http://dx.doi.org/10.1051/rnd:19870410.
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Lorain, P., J. Boujenah, A. Bricou, A. Benbara, and L. Carbillon. "Disproportion fœto-placentaire à terme : physiologique ou pathologique." Journal de Gynécologie Obstétrique et Biologie de la Reproduction 45, no. 5 (May 2016): 502–8. http://dx.doi.org/10.1016/j.jgyn.2015.06.021.
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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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Levy, RA, E. Avvad, J. Oliveira, and LC Porto. "Placental pathology in antiphospholipid syndrome." Lupus 7, no. 2_suppl (February 1998): 81–85. http://dx.doi.org/10.1177/096120339800700218.
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One of the major targets of antiphospholipid antibodies (aPL) is the placenta, the evolution of which during pregnancy has been well documented. Histopathological findings are related to gestational age, and several physiologic and pathologic alterations that occur during its development. The major findings in placentae from aPL positive patients are thrombosis, acute atherosis, a decreased number of syncytio-vascular membranes, increased number of syncytial knots and obliterative arteriopathy. These findings are not specific to the antiphospholipid syndrome (APS) and sometimes do not correlate with the fetal outcome. Histopathological study of placentae may elucidate mechanisms of action of aPL in fetal loss and other obstetric complications. In addition, it may assist in the investigation of the differential diagnosis between APS and pregnancy-induced hypertension. Immunohistochemical studies of local placental proteins contribute to this differential diagnosis.
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Guerrero Corrales, Yesenia, and Edgar Alberto Jorge Chang. "Placentary chorioangioma, perinatal management, report of two clinical cases." Journal of Pediatrics & Neonatal Care 15, no. 1 (2025): 31–34. https://doi.org/10.15406/jpnc.2025.15.00578.
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Introduction: Several cases of chorioangiomas have been described, however, there is little or no bibliography about the neonatal management of children born to mothers with this condition. Therefore, it is of utmost importance to have an approach to this type of pathology in order to venture a little more in the possible optimal management of these patients. Clinical case: Two patients with high cardiac output, who were given a high cardiovascular risk profile, however, extreme measures were taken at birth, especially physiological clamping of the umbilical cord, which improved cardiac output according to the decrease in vascular resistance at birth, improving the outcome of the patients, with minimal requirements for ventilatory support and short in-hospital stays. Conclusions: Physiologic clamping is a practice that should be made routine in patients with this prenatal history, who show combined cardiac output and elevated cardiovascular risk.
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Oyedele, Akinyemi, Morakinyo Oyedele, and Andrey V. Murashko. "Nursing profoundly premature newborns with artificial placentae: a review." V.F.Snegirev Archives of Obstetrics and Gynecology 8, no. 4 (December 15, 2021): 185–90. http://dx.doi.org/10.17816/2313-8726-2021-8-4-185-190.
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Neonatal mortality and morbidity are substantial issues affecting the maternal healthcare sector. Extremely premature infants, notably those born before the 28-week mark, experience significant morbidity and mortality rates during neonatal care. This is a result of developmental immaturity and iatrogenic injury. Several attempts have been made to develop a womb-like environment to mimic uteroplacental physiology, but limited success has been noted over the last decade. This review aims to summarize the current literature on improved techniques implemented in creating an artificial placenta, the principles of these procedures, and their limitations. Our findings indicate that implementing techniques that closely mimic uteroplacental pathophysiology is crucial in decreasing the excessive neonatal mortality and morbidity rates seen in extremely premature infants.
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Chaouat, G., and J. P. Kolb. "Immunoactive products of placenta. IV. Impairment by placental cells and their products of CTL function at effector stage." Journal of Immunology 135, no. 1 (July 1, 1985): 215–22. http://dx.doi.org/10.4049/jimmunol.135.1.215.
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Abstract Trophoblast-enriched cell suspensions prepared by collagenase digestion from midterm murine placentae were found resistant to CTL-mediated lysis. Treatment of such cells by trypsin or neuraminidase rendered these cells susceptible to such lytic effectors. Collagenase-prepared cell suspensions could impair CTL action, whereas neuraminidase- or trypsin-treated cells did not retain this property. This effect was also observed with extracts. These results indicate that soluble factors (which we will characterize in another paper) released by trophoblast cells (in fact, spongiotrophoblast) can interfere in a dose-dependent fashion with the action of lytic effectors. We suggest that such active mechanisms are physiologic components of the placental barrier and might be defective in some cases of immunologic abortions.
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Shahnawaz, Saira, Usman Shah Nawaz, Jonas Zaugg, Ghulam Hussain, Nadia Malik, Muhammad Zahoor-ul-Hassan Dogar, Shoaib Ahmad Malik, and Christiane Albrecht. "Dysregulated Autophagy Leads to Oxidative Stress and Aberrant Expression of ABC Transporters in Women with Early Miscarriage." Antioxidants 10, no. 11 (October 30, 2021): 1742. http://dx.doi.org/10.3390/antiox10111742.
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Early miscarriage (EMC) is a devastating obstetrical complication. ATP-binding cassette (ABC) transporters mediate cholesterol transfer across the placenta and enhance cell survival by effluxing substrates from target cells in the presence of stressors. Recent evidence reports an intricate interplay between autophagy and ABC transporters. We hypothesized that dysregulated autophagy and oxidative stress (OS) in the placenta leads to abnormal expression of membrane transporters contributing to poor pregnancy survival in EMC. We determined mRNA and protein expression of autophagy genes (Beclin-1/Bcl-2/LC3I/LC3II/p62) and ABC transporters (ABCA1/ABCG1/ABCG2) in placentae from EMC patients (n = 20), term controls (n = 19), first trimester (n = 6), and term controls (n = 5) controls. Oxidative/antioxidant status and biomarkers of oxidative damage were evaluated in maternal serum and placentae from EMC and healthy controls. In EMC, placental expression of LC3II/LC3I as well as of the key autophagy regulatory proteins Beclin-1 and Bcl-2 were reduced, whereas p62 was increased. Both in the serum and placentae of EMC patients, total OS was elevated reflected by increased oxidative damage markers (8-OHdG/malondialdehyde/carbonyl formation) accompanied by diminished levels of total antioxidant status, catalase, and total glutathione. Furthermore, we found reduced ABCG1 and increased ABCG2 expression. These findings suggest that a decreased autophagy status triggers Bcl-2-dependent OS leading to macromolecule damage in EMC placentae. The decreased expression of ABCG1 contributes to reduced cholesterol export to the growing fetus. Increasing ABCG2 expression could represent a protective feedback mechanism under inhibited autophagy conditions. In conclusion, dysregulated autophagy combined with increased oxidative toxicity and aberrant expression of placental ABC transporters affects materno-fetal health in EMC.
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Van Dyke, James U., Matthew C. Brandley, and Michael B. Thompson. "The evolution of viviparity: molecular and genomic data from squamate reptiles advance understanding of live birth in amniotes." REPRODUCTION 147, no. 1 (January 2014): R15—R26. http://dx.doi.org/10.1530/rep-13-0309.
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Squamate reptiles (lizards and snakes) are an ideal model system for testing hypotheses regarding the evolution of viviparity (live birth) in amniote vertebrates. Viviparity has evolved over 100 times in squamates, resulting in major changes in reproductive physiology. At a minimum, all viviparous squamates exhibit placentae formed by the appositions of maternal and embryonic tissues, which are homologous in origin with the tissues that form the placenta in therian mammals. These placentae facilitate adhesion of the conceptus to the uterus as well as exchange of oxygen, carbon dioxide, water, sodium, and calcium. However, most viviparous squamates continue to rely on yolk for nearly all of their organic nutrition. In contrast, some species, which rely on the placenta for at least a portion of organic nutrition, exhibit complex placental specializations associated with the transport of amino acids and fatty acids. Some viviparous squamates also exhibit reduced immunocompetence during pregnancy, which could be the result of immunosuppression to protect developing embryos. Recent molecular studies using both candidate-gene and next-generation sequencing approaches have suggested that at least some of the genes and gene families underlying these phenomena play similar roles in the uterus and placenta of viviparous mammals and squamates. Therefore, studies of the evolution of viviparity in squamates should inform hypotheses of the evolution of viviparity in all amniotes, including mammals.
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Fedorova, Olga V., Natalia I. Tapilskaya, Anton M. Bzhelyansky, Elena V. Frolova, Elena R. Nikitina, Vitaly A. Reznik, Vladimir A. Kashkin, and Alexei Y. Bagrov. "Interaction of Digibind with endogenous cardiotonic steroids from preeclamptic placentae." Journal of Hypertension 28, no. 2 (February 2010): 361–66. http://dx.doi.org/10.1097/hjh.0b013e328333226c.
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Bartczak-Rutkowska, Agnieszka, Lidia Tomkiewicz-Pająk, Katarzyna Kawka-Paciorkowska, Natalia Bajorek, Aleksandra Ciepłucha, Mariola Ropacka-Lesiak, and Olga Trojnarska. "Pregnancy Outcomes in Women after the Fontan Procedure." Journal of Clinical Medicine 12, no. 3 (January 18, 2023): 783. http://dx.doi.org/10.3390/jcm12030783.
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Women with single ventricle physiology after the Fontan procedure, despite numerous possible complications, can reach adulthood and give birth. Pregnancy poses a hemodynamic burden for distorted physiology of Fontan circulation, but according to the literature, it is usually well tolerated unless the patient is a “failing” Fontan. Our study aimed to assess maternal and fetal outcomes in patients after the Fontan procedure followed up in two tertiary Polish medical centers. We retrospectively evaluated all pregnancies in women after the Fontan procedure who were followed up between 1995–2022. During the study period, 15 women after the Fontan procedure had 26 pregnancies. Among 26 pregnancies, eleven ended with miscarriages, and 15 pregnancies resulted in 16 live births. Fetal complications were observed in 9 (56.3%) live births, with prematurity being the most common complication (n = 7, 43.8%). We recorded 3 (18.8%) neonatal deaths. Obstetrical complications were present in 6 (40%) out of 15 completed pregnancies—two (13.3%) cases of abruptio placentae, two (13.3%) pregnancies with premature rupture of membranes, and two (13.3%) patients with antepartum hemorrhage. There was neither maternal death nor heart failure decompensation during pregnancy. In two (13.3%) women, atrial arrhythmia developed. One (6.7%) patient in the second trimester developed ventricular arrhythmia. None of the patients suffered from systemic thromboembolism during pregnancy. Pregnancy in women after the Fontan procedure is well tolerated. However, it is burdened by a high risk of miscarriage and multiple obstetrical complications. These women require specialized care provided by both experienced cardiologists and obstetricians.
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Karl, Florian, and Didier Raboisson. "Stress thermique chez les bovins : bases physiopathologiques." Le Nouveau Praticien Vétérinaire élevages & santé 13, no. 50 (2021): 13–21. http://dx.doi.org/10.1051/npvelsa/50013.
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Les bovins, animaux homéothermes, présentent une zone de thermoneutralité. Lorsque cette zone est dépassée, la température corporelle augmente et une dépense d’énergie supplémentaire, par rapport à l’entretien, est nécessaire pour restaurer la température corporelle physiologique. L’ensemble des paramètres extérieurs entraînant ce processus constitue ce que l’on appelle le stress thermique. Le THI (index température-humidité) permet d’établir un seuil à partir duquel la vache est soumise à un stress thermique. Les réponses physiologiques visent à une réduction de la production de chaleur (diminution de l’ingestion, baisse du métabolisme), et à une élimination de celle-ci (vasodilatation, transpiration, augmentation de la fréquence respiratoire). Le stress thermique a des conséquences multiples sur les bovins : baisse d’immunité, augmentation des infections, baisse de production laitière et impact sur la qualité du lait (baisse des taux protéique et taux butyreux, augmentation des comptages cellulaires, augmentation de l’incidence des mammites cliniques), dégradation de la reproduction, baisse de croissance des veaux. Ces indicateurs, faciles à mesurer sur le terrain, s’expliquent en particulier par un remaniement des équilibres hormonaux liés à l’exposition des vaches à la chaleur. L’hormone de croissance et les hormones thyroïdiennes, responsables d’une production de chaleur indirecte, sont diminuées. A contrario, les glucocorticoïdes, vasodilatateurs, favorisent la dissipation de chaleur et les vaches présentent une augmentation de la glucocortisolémie. Les veaux issus de mères exposées à un stress thermique sont, quant à eux, soumis au stade fœtal à différentes modifications (baisse de la fonction placentaire, augmentation de la température fœtale, baisse de croissance des tissus fœtaux, …), ayant plusieurs conséquences (augmentation de la mortalité, poids plus faible à la naissance, production laitière plus faible, …).
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Irge, Emine, Zekai Halici, Mehmet Yilmaz, Elif Cadirci, and Emre Karakus. "Evaluation of 5-HT7receptor expression in the placentae of normal and pre-eclamptic women." Clinical and Experimental Hypertension 38, no. 2 (January 21, 2016): 189–93. http://dx.doi.org/10.3109/10641963.2015.1081215.
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Hnat, Michael, and Roger E. Bawdon. "Transfer of Meropenem in the ex Vivo Human Placenta perfusion Model." Infectious Diseases in Obstetrics and Gynecology 13, no. 4 (2005): 223–27. http://dx.doi.org/10.1155/2005/961356.
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Objectives.To determine maternal-fetal transplacental passage of meropenem in the ex vivo human perfusion model.Study design.Term placentae (n= 6) were collected immediately after delivery. A single cotyledon was localized, perfused and stabilized with physiologic Eagles minimal essential medium containing 3% bovine albumin and heparin as described by Chalier (Chalier JC. Criteria for evaluating perfusion experiments and presentation results. Contrib Gynecol Obstet 1985; 13:32–39). Meropenem was added to the maternal medium in concentrations similar to maternal serum peak and trough levels, then perfused through the maternal circulation of the cotyledon. To assess transfer and accumulation, fluid aliquots from both the maternal and fetal compartments were collected over an hour at defined intervals in an open and closed system. AntipyrineC14was added to the medium in order to calculate the transport fraction and clearance indexes. Meropenem and antipyrineC14concentrations were determined by High-pressure Liquid Chromatography and liquid scintillation, respectively.Results.Mean antipyrine transport fraction was 2.33 + 0.25. Maternal and fetal mean meropenem peak concentrations were 54.3 + 3.3μg/ml and 2.2 + 0.18μg/ml, respectively. Whereas, maternal and fetal mean trough concentrations were 12.7 + 1.3μg/ml and 0.41 + 0.10μg/ml, respectively. Mean peak clearance index was 0.077 + 0.007 and the mean trough was 0.052 + 0.015. Mean accumulation for the peak and trough concentrations of meropenem were 0.9 and 2.95μg/ml, respectively.Conclusions.Transplacental passage of meropenem was incomplete in the ex vivo human placental perfusion model. Accumulation was also noted in the fetal compartment
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Adhikari, Anil Kumar, Mahuya Dutta, S. K. Samim Ferdows, Madhu Jain, and Jyoti Shukla. "Prevalence and significance of thrombophilia markers in adverse pregnancy outcome." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 6, no. 2 (January 31, 2017): 489. http://dx.doi.org/10.18203/2320-1770.ijrcog20170368.
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Background: Thrombophilia complicates the pregnancy by interfering the physiology of utero-placental circulation which in turn leads to IUGR, IUD, PIH, RPL, abruption placentae. This study is to find out the prevalence and significance of different thrombophilia markers in cases of adverse pregnancy outcome in eastern part of Uttar Pradesh, India.Methods: 54 antenatal women are selected from the cases presented with or previous history of PIH, IUGR, IUD, Abruption or early/late abortion. A thorough family history, history of risk factors, clinical examination were noted. Platelet count, prothrombin time(PT), activated partial thromboplastin time (APTT), plasma fibrinogen, factor-VIII assay, LA, ACLA, protein- C, protein- S, TORCH, thyroid profile, blood sugar, USG is done in all patients at the time of first registration. 50 antenatal females without any bad obstetric history was taken as controls.Results: Among 54 cases, 64.8% cases were positive for thrombophilia markers, whereas 6% control had presence of thrombophilia markers. 6.5% thrombophilia positive cases had ≥3 markers present and had ≥2 manifestations of adverse pregnancy outcome in 100% cases. Prevalence of different thrombophilia markers are studied in individual case and association to various outcomes were noted.Conclusions: There was high prevalence of thrombophilia markers in the cases with adverse pregnancy outcome. As treatment was found significantly effective in literature, screening of these markers should be done in patients with bad obstetric history.
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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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Jakoubek, Vít, Jana Bíbová, Jan Herget, and Václav Hampl. "Chronic hypoxia increases fetoplacental vascular resistance and vasoconstrictor reactivity in the rat." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 4 (April 2008): H1638—H1644. http://dx.doi.org/10.1152/ajpheart.01120.2007.
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An increase in fetoplacental vascular resistance caused by hypoxia is considered one of the key factors of placental hypoperfusion and fetal undernutrition leading to intrauterine growth restriction (IUGR), one of the serious problems in current neonatology. However, although acute hypoxia has been shown to cause fetoplacental vasoconstriction, the effects of more sustained hypoxic exposure are unknown. This study was designed to test the hypothesis that chronic hypoxia elicits elevations in fetoplacental resistance, that this effect is not completely reversible by acute reoxygenation, and that it is accompanied by increased acute vasoconstrictor reactivity of the fetoplacental vasculature. We measured fetoplacental vascular resistance as well as acute vasoconstrictor reactivity in isolated perfused placentae from rats exposed to hypoxia (10% O2) during the last week of a 3-wk pregnancy. We found that chronic hypoxia shifted the relationship between perfusion pressure and flow rate toward higher pressure values (by ∼20%). This increased vascular resistance was refractory to a high dose of sodium nitroprusside, implying the involvement of other factors than increased vascular tone. Chronic hypoxia also increased vasoconstrictor responses to angiotensin II (by ∼75%) and to acute hypoxic challenges (by >150%). We conclude that chronic prenatal hypoxia causes a sustained elevation of fetoplacental vascular resistance and vasoconstrictor reactivity that are likely to produce placental hypoperfusion and fetal undernutrition in vivo.
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Ietta, Francesca, Yuanhong Wu, Roberta Romagnoli, Nima Soleymanlou, Barbara Orsini, Stacy Zamudio, Luana Paulesu, and Isabella Caniggia. "Oxygen regulation of macrophage migration inhibitory factor in human placenta." American Journal of Physiology-Endocrinology and Metabolism 292, no. 1 (January 2007): E272—E280. http://dx.doi.org/10.1152/ajpendo.00086.2006.
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Macrophage migration inhibitory factor (MIF) is an important proinflammatory cytokine involved in regulation of macrophage function. In addition, MIF may also play a role in murine and human reproduction. Although both first trimester trophoblast and decidua express MIF, the regulation and functional significance of this cytokine during human placental development remains unclear. We assessed MIF expression throughout normal human placental development, as well as in in vitro (chorionic villous explants) and in vivo (high altitude placentae) models of human placental hypoxia. Dimethyloxalylglycine (DMOG), which stabilizes hypoxia inducible factor-1 under normoxic conditions, was also used to mimic the effects of hypoxia on MIF expression. Quantitative real-time PCR and Western blot analysis showed high MIF protein and mRNA expression at 7–10 wk and lower levels at 11–12 wk until term. Exposure of villous explants to 3% O2 resulted in increased MIF expression and secretion relative to standard conditions (20% O2). DMOG treatment under 20% O2 increased MIF expression. In situ hybridization and immunohistochemistry showed elevated MIF expression in low oxygen-induced extravillous trophoblast cells. Finally, a significant increase in MIF transcript was observed in placental tissues from high-altitude pregnancies. Hence, three experimental models of placental hypoxia (early gestation, DMOG treatment, and high altitude) converge in stimulating increased MIF, supporting the conclusion that placental-derived MIF is an oxygen-responsive cytokine highly expressed in physiological in vivo and in in vitro low oxygen conditions.
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Maeda, Kenji J., Kurt C. Showmaker, Ashley C. Johnson, Michael R. Garrett, and Jennifer M. Sasser. "Spontaneous superimposed preeclampsia: chronology and expression unveiled by temporal transcriptomic analysis." Physiological Genomics 51, no. 8 (August 1, 2019): 342–55. http://dx.doi.org/10.1152/physiolgenomics.00020.2019.
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Preeclampsia (PE), a multifactorial pregnancy-specific syndrome accounting for up to 8% of pregnancy complications, is a leading cause of maternal and fetal morbidity and mortality. PE is also associated with long-term risk of hypertension and stroke for both mother and fetus. Currently, the only “cure” is delivery of the baby and placenta, largely because the pathogenesis of PE is not yet fully understood. PE is associated with impaired vascular remodeling at the maternal-fetal interface and placental insufficiency; however, specific factors contributing to this impairment have not been identified. To identify molecular pathways involved in PE, we examined temporal transcriptomic changes occurring within the uterus, uterine implantation sites, and placentae from the Dahl salt-sensitive (Dahl S) rat model of superimposed PE compared with Sprague Dawley (SD) rats. We hypothesized that targeted gene analysis and whole transcriptome analysis would identify genetic factors that contribute to development of the preeclamptic phenotype in the Dahl S rat and unveil novel biomarkers, therapeutic targets, and mechanistic pathways in PE. Quantitative real-time PCR (qRT-PCR) and whole genome microarray analysis were performed on isolated total RNA from uterus ( day 0), uterine implantation sites ( days 7 and 10), and placenta ( days 14 and 20). We found 624, 332, 185, and 366 genes to be differentially expressed between Dahl S (PE) and SD (normal pregnancy) on days 0, 7, 10, and 14, respectively. Our data revealed numerous pathways that may play a role in the pathophysiology of spontaneous superimposed PE and allow for further investigation of novel therapeutic targets and biomarker development.
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Peiris, Hassendrini N., Anna P. Ponnampalam, Claire C. Osepchook, Murray D. Mitchell, and Mark P. Green. "Placental expression of myostatin and follistatin-like-3 protein in a model of developmental programming." American Journal of Physiology-Endocrinology and Metabolism 298, no. 4 (April 2010): E854—E861. http://dx.doi.org/10.1152/ajpendo.00673.2009.
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Maternal undernutrition during gestation is known to be detrimental to fetal development, leading to a propensity for metabolic disorders later in the adult lives of the offspring. Identifying possible mediators and physiological processes involved in modulating nutrient transport within the placenta is essential to prevent and/or develop treatments for the effects of aberrant nutrition, nutrient transfer, and detrimental changes to fetal development. A potential role for myostatin as a mediator of nutrient uptake and transport from the mother to the fetus was shown through the recent finding that myostatin acts within the human placenta to modulate glucose uptake and therefore homeostasis. The mRNA and protein expression of myostatin and its inhibitor, follistatin-like-3 (FSTL3), was studied in the placenta and skeletal muscle of a transgenerational Wistar rat model of gestational maternal undernutrition in which the F2 offspring postweaning consumed a high-fat (HF) diet. Alterations in placental characteristics and offspring phenotype, specifically glucose homeostasis, were evident in the transgenerationally undernourished (UNAD) group. Myostatin and FSTL3 protein expression were also higher ( P < 0.05) in the placentae of the UNAD compared with the control group. At maturity, UNAD HF-fed animals had higher ( P < 0.05) skeletal muscle expression of FSTL3 than control animals. In summary, maternal undernutrition during gestation results in the aberrant regulation of myostatin and FSTL3 in the placenta and skeletal muscle of subsequent generations. Myostatin, through the disruption of maternal nutrient supply to the fetus, may thus be a potential mediator of offspring phenotype.
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Sahay, Akriti S., Anjali T. Jadhav, Deepali P. Sundrani, Girija N. Wagh, and Sadhana R. Joshi. "Differential Expression of Nerve Growth Factor (NGF) and Brain Derived Neurotrophic Factor (BDNF) in Different Regions of Normal and Preeclampsia Placentae." Clinical and Experimental Hypertension 42, no. 4 (September 14, 2019): 360–64. http://dx.doi.org/10.1080/10641963.2019.1665677.
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Buddle, Alice L., James U. Van Dyke, Michael B. Thompson, Colin A. Simpfendorfer, Christopher R. Murphy, Margot L. Day, and Camilla M. Whittington. "Structure and permeability of the egg capsule of the placental Australian sharpnose shark, Rhizoprionodon taylori." Journal of Comparative Physiology B 192, no. 2 (February 4, 2022): 263–73. http://dx.doi.org/10.1007/s00360-021-01427-0.
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AbstractShark placentae are derived from modifications to the fetal yolk sac and the maternal uterine mucosa. In almost all placental sharks, embryonic development occurs in an egg capsule that remains intact for the entire pregnancy, separating the fetal tissues from the maternal tissues at the placental interface. Here, we investigate the structure and permeability of the egg capsules that surround developing embryos of the placental Australian sharpnose shark (Rhizoprionodon taylori) during late pregnancy. The egg capsule is an acellular fibrous structure that is 0.42 ± 0.04 μm thick at the placental interface between the yolk sac and uterine tissues, and 0.67 ± 0.08 μm thick in the paraplacental regions. This is the thinnest egg capsule of any placental shark measured so far, which may increase the diffusion rate of respiratory gases, fetal wastes, water and nutrients between maternal and fetal tissues. Molecules smaller than or equal to ~ 1000 Da can diffuse through the egg capsule, but larger proteins (~ 3000–26,000 Da) cannot. Similar permeability characteristics between the egg capsule of R. taylori and other placental sharks suggest that molecular size is an important determinant of the molecules that can be exchanged between the mother and her embryos during pregnancy.
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Sawa, Hiroki, Hiroyuki Ukita, Minoru Fukuda, Hajime Kamada, Isamu Saito, and Björn öbrink. "Spatiotemporal Expression of C-CAM in the Rat Placenta." Journal of Histochemistry & Cytochemistry 45, no. 7 (July 1997): 1021–34. http://dx.doi.org/10.1177/002215549704500711.
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We investigated the expression of the immunoglobulin superfamily cell adhesion molecule, C-CAM, in developing and mature rat placenta. By immunohistochemical staining at the light microscopic level, no C-CAM-expression was seen before Day 9 of gestation, when it appeared in the trophoblasts of ectoplacental cones. On Day 10.5, spongiotrophoblasts and invasive trophoblasts around the maternal vessels of the decidua basalis were stained positively. On Day 12.5, C-CAM was detected in the spongiotrophoblasts of the junctional layer, but labyrinth trophoblasts and secondary giant trophoblasts were not stained. On Day 17.5, C-CAM was found only in the labyrinth and lacunae of the junctional layer. At this stage, both the labyrinth cytotrophoblasts of the maternal blood vessels and the endothelial cells of the embryonic capillaries were strongly stained. Placental tissues from gestational Days 12.5 and 17.5 were analyzed by immunoelectron microscopy to determine the location of C-CAM at the subcellular level. On Day 12.5, positive staining of the spongiotrophoblasts was observed, mainly on surface membranes and microvilli between loosely associated cells. On Day 17.5, staining was found primarily on the microvilli of the maternal luminal surfaces of the labyrinth cytotrophoblasts, and both on the luminal surface and in the cytoplasm of endothelial cells of the embryonic vessels. RT-PCR analysis and Southern blotting of the PCR products revealed expression of mRNA species for both of the major isoforms, C-CAM1 and C-CAM2. Immunoblotting analysis of C-CAM isolated from 12.5-day and 14.5-day placentae showed that it appeared as a broad band with an apparent molecular mass of 110–170 kD. In summary, C-CAM was strongly expressed in a specific spatiotemporal pattern in trophoblasts actively involved in formation of the placental tissue, suggesting an important role in placental development. In the mature placenta, C-CAM expression was confined to the trophoblastic and endothelial cells lining the maternal and embryonic vessels, respectively, suggesting important functions in placental physiology.
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Thompson, M. B., B. K. Speake, J. R. Stewart, K. J. Russell, R. J. McCartney, and P. F. Surai. "Placental nutrition in the viviparous lizard Niveoscincus metallicus: the influence of placental type." Journal of Experimental Biology 202, no. 21 (November 1, 1999): 2985–92. http://dx.doi.org/10.1242/jeb.202.21.2985.
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The ion, energy, lipid, nitrogen and fat-soluble vitamin contents of freshly ovulated eggs and neonates of the viviparous lizard Niveoscincus metallicus were measured to quantify uptake of nutrients across the placenta. This species is particularly interesting because it has a chorio-allantoic placenta that is intermediate in complexity compared to viviparous species that have been the focus of other studies. Newly ovulated eggs have a wet mass of 79.6+/−4.6 mg and a dry mass of 41.8+/−2.8 mg, compared to the neonates that have a wet mass of 224.2+/−8.2 mg and dry mass of 37.9+/−1.2 mg. Thus, there is no significant net uptake of dry matter across the placenta. Neonates have significantly less lipid (6.2+/−0.4 mg) than eggs (12.7+/−0.5 mg), but no significant difference in nitrogen (4.1+/−0.3 mg) compared to eggs (4.5+/−0.2 mg). Energy densities reflect the protein and lipid composition and the relative dry masses of the eggs and neonates. There is significantly more energy (1029.1+/−80.0 J) in the egg than in the neonate (858.2+/−38.6 J). The increase in the ash content of the neonates (2.9+/−0.2 mg) compared to fresh eggs (2.1+/−0.3 mg) was not significant, even though there was an approximately threefold increase in the amount of sodium (0.11+/−0.01 mg in neonates, 0.34+/−0.01 mg in eggs) and potassium (0.12+/−0.017 in neonates, 0.40+/−0.01 mg in eggs) in neonates compared to eggs. There was no significant uptake of calcium and magnesium during development. The egg lipids consisted of triacylglycerol (66.7+/−2.3 %), phospholipid (18.9+/−0.7 %), cholesteryl ester (4.9+/−1.6 %) and free cholesterol (5.6+/−1.5 %). The egg phospholipid contained comparatively high proportions of arachidonic and eicosapentanoic acids but low levels of docosahexaenoic acid (DHA), whereas the phospholipid of the neonate was greatly enriched in DHA. In the egg, the predominant vitamin E was (α)-tocopherol (62.6+/−3.4 mg g(−)(1)), although there was some (γ)-tocotrienol (3.5+/−0.3 mg g(−)(1)), and vitamin A was present (1.5+/−0.2 mg g(−)(1)). The ratio of neonate dry mass to egg dry mass of N. metallicus (0.91) lies between that of species with type I (0.78) and type III (1.70) chorio-allantoic placentae, confirming our conclusion that the placenta of N. metallicus is functionally intermediate, as well as intermediate in complexity, between these other two types.
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K, Rajkumar, Geena Augustine, and Jithesh K. "Histological alterations of the placenta in gestational diabetes mellitus: Implications for fetoplacental transport and fetal outcome." National Journal of Physiology, Pharmacy and Pharmacology, 2023, 1. http://dx.doi.org/10.5455/njppp.2023.13.09468202323102023.
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Background: The placenta is a pivotal medium for physiological exchanges between the maternal and fetal circulations. However, diabetic insults early in gestation can influence the placental barrier, potentially impacting fetal development and outcomes. This study sought to understand the histological changes in the placentae of gestational diabetes mellitus (GDM) cases, highlighting the significance of these alterations on fetal health. Aims and Objectives: The primary aim of this research was to elucidate the histological changes present in the placentae of women diagnosed with GDM. Furthermore, the study sought to determine the implications of these changes on the standard placental anatomy and its associated functionalities, thereby assessing potential impacts on fetal development and outcomes. Materials and Methods: A case–control study was conducted at MES Medical College, Perinthalmanna, Kerala, from October 2014 to December 2018. Inclusion criteria considered pregnant women aged 19–38 years diagnosed with GDM, among other factors. Exclusion criteria weeded out pre-diagnosed diabetes cases, unclear glycemic statuses, and a range of pregnancy complications. Placentae samples underwent meticulous histological and histochemical analyses, focusing on key histological features, including syncytiotrophoblastic knots, vasculosyncytial membranes, and chorangiosis. Results: Significant histological variations were observed in GDM cases compared to controls. Notably, there was an increased formation of syncytial knots and reduced vasculosyncytial membranes in GDM placentae. In addition, chorangiosis was more prevalent, suggesting potential chronic prenatal hypoxia. Marked thickening of the syncytiotrophoblast basement membrane, villous edema, and fibrinoid necrosis were other pertinent findings in GDM cases, each with statistical significance (P < 0.001). Conclusion: The findings underscore the profound histological changes in the placenta associated with GDM, emphasizing the need for comprehensive maternal care and monitoring. These alterations can compromise fetoplacental transport and may have long-term implications on fetal health, highlighting the critical role of timely GDM diagnosis and intervention.
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Gillmore, Taylor, Abby Farrell, Sruthi Alahari, Julien Sallais, Merve Kurt, Chanho Park, Jonathan Ausman, Michael Litvack, Martin Post, and Isabella Caniggia. "Dichotomy in hypoxia-induced mitochondrial fission in placental mesenchymal cells during development and preeclampsia: consequences for trophoblast mitochondrial homeostasis." Cell Death & Disease 13, no. 2 (February 2022). http://dx.doi.org/10.1038/s41419-022-04641-y.
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AbstractDynamic changes in physiologic oxygen are required for proper placenta development; yet, when low-oxygen levels persist, placental development is halted, culminating in preeclampsia (PE), a serious complication of pregnancy. Considering mitochondria’s function is intimately linked to oxygen changes, we investigated the impact of oxygen on mitochondrial dynamics in placental mesenchymal stromal cells (pMSCs) that are vital for proper placental development. Transmission electron microscopy, proximity ligation assays for mitochondrial VDAC1 and endoplasmic reticulum IP3R, and immunoanalyses of p-DRP1 and OPA1, demonstrate that low-oxygen conditions in early 1st trimester and PE promote mitochondrial fission in pMSCs. Increased mitochondrial fission of mesenchymal cells was confirmed in whole PE placental tissue sections. Inhibition of DRP1 oligomerization with MDiVi-1 shows that low oxygen-induced mitochondrial fission is a direct consequence of DRP1 activation, likely via HIF1. Mitophagy, a downstream event prompted by mitochondrial fission, is a prominent outcome in PE, but not 1st trimester pMSCs. We also investigated whether mesenchymal–epithelial interactions affect mitochondrial dynamics of trophoblasts in PE placentae. Exposure of trophoblastic JEG3 cells to exosomes of preeclamptic pMSCs caused heightened mitochondrial fission in the cells via a sphingomyelin-dependent mechanism that was restored by MDiVi-1. Our data uncovered dichotomous regulation of mitochondrial fission and health in human placental mesenchymal cells under physiologic and pathologic hypoxic conditions and its impact on neighboring trophoblast cells.
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Pillai, Reshma A., Mohammed O. Islam, Preben Selvam, Neha Sharma, Anne H. Y. Chu, Oliver C. Watkins, Keith M. Godfrey, Rohan M. Lewis, and Shiao Y. Chan. "Placental Inositol Reduced in Gestational Diabetes as Glucose Alters Inositol Transporters and IMPA1 Enzyme Expression." Journal of Clinical Endocrinology & Metabolism, November 9, 2020. http://dx.doi.org/10.1210/clinem/dgaa814.
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Abstract Context Perturbed inositol physiology in insulin-resistant conditions has led to proposals of inositol supplementation for gestational diabetes (GDM) prevention, but placental inositol biology is poorly understood. Objective Investigate associations of maternal glycemia with placental inositol content, determine glucose effects on placental expression of inositol enzymes and transporters, and examine relations with birthweight. Design and Participants Case-control study of placentae from term singleton pregnancies (GDM n = 24, non-GDM n = 26), and culture of another 9 placentae in different concentrations of glucose and myo-inositol for 48 hours. Main Outcome Measures Placental inositol was quantified by the Megazyme assay. Relative expression of enzymes involved in myo-inositol metabolism and plasma membrane inositol transport was determined by quantitative RT-PCR and immunoblotting. Linear regression analyses were adjusted for maternal age, body mass index, ethnicity, gestational age, and sex. Results Placental inositol content was 17% lower in GDM compared with non-GDM. Higher maternal mid-gestation glycemia were associated with lower placental inositol. Increasing fasting glycemia was associated with lower protein levels of the myo-inositol synthesis enzyme, IMPA1, and the inositol transporters, SLC5A11 and SLC2A13, the expression of which also correlated with placental inositol content. In vitro, higher glucose concentrations reduced IMPA1 and SLC5A11 mRNA expression. Increasing fasting glycemia positively associated with customized birthweight percentile as expected in cases with low placental inositol, but this association was attenuated with high placental inositol. Conclusion Glycemia-induced dysregulation of placental inositol synthesis and transport may be implicated in reduced placental inositol content in GDM, and this may in turn be permissive to accelerated fetal growth.
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Gomes, Viviane Cristine Leite, and Jenny L. Sones. "From Inhibition of Trophoblast Cell Invasion to Pro-apoptosis: What are the Potential Roles of Kisspeptins in Preeclampsia?" American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, May 19, 2021. http://dx.doi.org/10.1152/ajpregu.00258.2020.
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Preeclampsia (PE) is a life-threatening human gestational syndrome with incompletely understood etiopathogenesis. The disorder has a spectrum of clinical features, likely due to a complex interaction between maternal predisposing factors and abnormalities at the maternal-fetal interface. Poor trophoblast cell invasion, inadequate uterine vascular remodeling and placental hypoperfusion are considered key placental events leading to PE. Kisspeptins, a family of small peptides derived from the KISS1 gene, have been implicated in the development of this syndrome. Most studies of kisspeptin expression in PE have reported an upregulation of kisspeptins and/or their cognate receptor in preeclamptic placentae. Conversely, maternal peripheral blood concentration of kisspeptins is reportedly lower in PE than in uncomplicated pregnancies. This apparent paradox remains to be further elucidated. While kisspeptins were initially known for inhibiting cellular migration and invasion, other biological activities attributed to these peptides include neuroendocrine regulation of reproduction, metabolism regulation, inhibition of angiogenesis and induction of apoptosis. This review summarizes the current knowledge on expression and biological activity of kisspeptins at the maternal-fetal interface in the context of PE.
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Seedat, Faheem, Neva Kandzija, Michael J. Ellis, Shuhan Jiang, Asselzhan Sarbalina, James Bancroft, Edward Drydale, et al. "Placental small extracellular vesicles from normal pregnancy and gestational diabetes increase insulin gene transcription and content in β cells." Clinical Science, October 21, 2024. http://dx.doi.org/10.1042/cs20241782.
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Insulin secretion increases progressively during pregnancy to maintain normal maternal blood glucose levels. The placenta plays a crucial role in this process by releasing hormones and extracellular vesicles into the maternal circulation, which drive significant changes in pregnancy physiology. Placental extracellular vesicles, which are detectable in the plasma of pregnant women, have been shown to signal peripheral tissues and contribute to pregnancy-related conditions. While studies using murine models have demonstrated that extracellular vesicles can modulate insulin secretion in pancreatic islets, it remains unclear whether these effects translate to human biology. Understanding how placental signals enhance insulin synthesis and secretion from β cells could be pivotal in developing new therapies for diabetes. In our study, we isolated placental small extracellular vesicles from human placentae and utilised the human β cell line, EndoC-βH3, to investigate their effects on β-cell function in vitro. Our results indicate that human β cells internalise placental small extracellular vesicles, leading to enhanced insulin gene expression and increased insulin content within the β cells. Moreover, these vesicles upregulated the expression of Annexin A1, a protein known to increase insulin content. This upregulation of Annexin A1 holds promise as a potential mechanism by which placental small extracellular vesicles enhance insulin biosynthesis.
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Klein, Anders Bue, Pablo Ranea-Robles, Trine Sand Nicolaisen, Claudia Gil, Kornelia Johann, Julia Prats Quesada, Nina Pistoljevic, et al. "Cross-species comparison of pregnancy-induced GDF15." American Journal of Physiology-Endocrinology and Metabolism, August 16, 2023. http://dx.doi.org/10.1152/ajpendo.00134.2023.
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Growth differentiation factor 15 (GDF15) is a stress-induced cytokine. Although the exact physiological function of GDF15 is not yet fully comprehended, the significant elevation of circulating GDF15 levels during gestation suggests a potential role for this hormone in pregnancy. This is corroborated by genetic association studies in which GDF15 and the GDF15 receptor, GDNF Family Receptor Alpha Like (GFRAL) have been linked to morning sickness and hyperemesis gravidarum (HG) in humans. Here, we studied GDF15 biology during pregnancy in mice, rats, macaques, and humans. In contrast to macaques and humans, mice and rats exhibited an underwhelming induction in plasma GDF15 levels in response to pregnancy (~75-fold increase in macaques vs. ~2-fold increase in rodents). The changes in circulating GDF15 levels were corroborated by the magnitude of Gdf15 mRNA and GDF15 protein expression in placentae from mice, rats, and macaques. These species-specific findings may help guide future studies focusing on GDF15 in pregnancy and on the evaluation of pharmacological strategies to interfere with GDF15-GFRAL signaling to treat severe nausea and HG.
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Tehrani, Jesse M., Elizabeth M. Kennedy, Fu-Ying Tian, Todd M. Everson, Maya Deyssenroth, Amber Burt, Karen Hermetz, et al. "Variation in placental microRNA expression associates with maternal family history of cardiovascular disease." Journal of Developmental Origins of Health and Disease, July 11, 2022, 1–8. http://dx.doi.org/10.1017/s2040174422000319.
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Abstract In the United States, cardiovascular disease is the leading cause of death and the rate of maternal mortality remains among the highest of any industrialized nation. Maternal cardiometabolic health throughout gestation and postpartum is representative of placental health and physiology. Both proper placental functionality and placental microRNA expression are essential to successful pregnancy outcomes, and both are highly sensitive to genetic and environmental sources of variation. Placental pathologies, such as preeclampsia, are associated with maternal cardiovascular health but may also contribute to the developmental programming of chronic disease in offspring. However, the role of more subtle alterations to placental function and microRNA expression in this developmental programming remains poorly understood. We performed small RNA sequencing to investigate microRNA in placentae from the Rhode Island Child Health Study (n = 230). MicroRNA counts were modeled on maternal family history of cardiovascular disease using negative binomial generalized linear models. MicroRNAs were considered to be differentially expressed at a false discovery rate (FDR) less than 0.10. Parallel mRNA sequencing data and bioinformatic target prediction software were then used to identify potential mRNA targets of differentially expressed microRNAs. Nine differentially expressed microRNAs were identified (FDR < 0.1). Bioinformatic target prediction revealed 66 potential mRNA targets of these microRNAs, many of which are implicated in TGFβ signaling pathway but also in pathways involving cellular metabolism and immunomodulation. A robust association exists between familial cardiovascular disease and placental microRNA expression which may be implicated in both placental insufficiencies and the developmental programming of chronic disease.
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Schofield, Lachlan G., Richard G. S. Kahl, Samantha L. Rodrigues, Joshua J. Fisher, Saije K. Endacott, Sarah J. Delforce, Eugenie R. Lumbers, Jacinta H. Martin, and Kirsty G. Pringle. "Placental deficiency of the (pro)renin receptor ((P)RR) reduces placental development and functional capacity." Frontiers in Cell and Developmental Biology 11 (August 1, 2023). http://dx.doi.org/10.3389/fcell.2023.1212898.
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The (pro)renin receptor ((P)RR; also known as ATP6AP2) is a multifunctional receptor. The (P)RR activates the tissue renin-angiotensin system (RAS) and is also involved in regulating integral intracellular pathways such as V-ATPase and Wnt/β-catenin signalling. Given this, the (P)RR may be associated with essential pathways in placentation, however its role within the context of pregnancy remains poorly characterised. The first trimester/extravillous trophoblast cell line, HTR-8/SVneo, underwent an siRNA knockdown where they were incubated for 24 h with a negative control siRNA or siRNA targeting ATP6AP2 mRNA. xCELLigence real-time cell analysis was performed to assess the effect of ATP6AP2 mRNA knockdown on HTR-8/SVneo cell proliferation, migration, and invasion. In subsequent experiments, GFP-encoding lentiviral packaged gene-constructs were used to knockdown (P)RR expression in the trophectoderm of C57/BL6/CBA-F1 mouse blastocysts. Blastocysts were incubated for 6 h with vehicle (no-virus), control virus (non-targeting shRNA and GFP), or (P)RR-knockdown virus ((P)RR shRNA and GFP) before transfer into recipient pseudo-pregnant Swiss CD1 female mice. Fetal and placental tissues were collected and assessed at embryonic age (EA) 10 and 18. (P)RR levels were measured in the labyrinth zone of day 18 placentae and stereological Merz grid analysis was performed to determine the volumetric distribution of trophoblasts, fetal capillaries, and the maternal blood space. We showed that a reduction of ATP6AP2 expression in HTR-8/SVneo cells in vitro, impaired trophoblast proliferation, migration, and invasion. In vivo, decreasing placental labyrinth (P)RR expression adversely effected placental physiology, decreasing placental trophoblast number and total surface area available for exchange, while also increasing maternal blood space. Additionally, decreased (P)RR affected placental efficacy evident by the reduced fetal-placental weight ratio. Our study shows that the (P)RR is necessary for appropriate placental development and function.
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Kitase, Yuma, Nethra K. Madurai, Sarah Hamimi, Ryan L. Hellinger, O. Angel Odukoya, Sindhu Ramachandra, Sankar Muthukumar, et al. "Chorioamnionitis disrupts erythropoietin and melatonin homeostasis through the placental-fetal-brain axis during critical developmental periods." Frontiers in Physiology 14 (July 20, 2023). http://dx.doi.org/10.3389/fphys.2023.1201699.
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Introduction: Novel therapeutics are emerging to mitigate damage from perinatal brain injury (PBI). Few newborns with PBI suffer from a singular etiology. Most experience cumulative insults from prenatal inflammation, genetic and epigenetic vulnerability, toxins (opioids, other drug exposures, environmental exposure), hypoxia-ischemia, and postnatal stressors such as sepsis and seizures. Accordingly, tailoring of emerging therapeutic regimens with endogenous repair or neuro-immunomodulatory agents for individuals requires a more precise understanding of ligand, receptor-, and non-receptor-mediated regulation of essential developmental hormones. Given the recent clinical focus on neurorepair for PBI, we hypothesized that there would be injury-induced changes in erythropoietin (EPO), erythropoietin receptor (EPOR), melatonin receptor (MLTR), NAD-dependent deacetylase sirtuin-1 (SIRT1) signaling, and hypoxia inducible factors (HIF1α, HIF2α). Specifically, we predicted that EPO, EPOR, MLTR1, SIRT1, HIF1α and HIF2α alterations after chorioamnionitis (CHORIO) would reflect relative changes observed in human preterm infants. Similarly, we expected unique developmental regulation after injury that would reveal potential clues to mechanisms and timing of inflammatory and oxidative injury after CHORIO that could inform future therapeutic development to treat PBI.Methods: To induce CHORIO, a laparotomy was performed on embryonic day 18 (E18) in rats with transient uterine artery occlusion plus intra-amniotic injection of lipopolysaccharide (LPS). Placentae and fetal brains were collected at 24 h. Brains were also collected on postnatal day 2 (P2), P7, and P21. EPO, EPOR, MLTR1, SIRT1, HIF1α and HIF2α levels were quantified using a clinical electrochemiluminescent biomarker platform, qPCR, and/or RNAscope. MLT levels were quantified with liquid chromatography mass spectrometry.Results: Examination of EPO, EPOR, and MLTR1 at 24 h showed that while placental levels of EPO and MLTR1 mRNA were decreased acutely after CHORIO, cerebral levels of EPO, EPOR and MLTR1 mRNA were increased compared to control. Notably, CHORIO brains at P2 were SIRT1 mRNA deficient with increased HIF1α and HIF2α despite normalized levels of EPO, EPOR and MLTR1, and in the presence of elevated serum EPO levels. Uniquely, brain levels of EPO, EPOR and MLTR1 shifted at P7 and P21, with prominent CHORIO-induced changes in mRNA expression. Reductions at P21 were concomitant with increased serum EPO levels in CHORIO rats compared to controls and variable MLT levels.Discussion: These data reveal that commensurate with robust inflammation through the maternal placental-fetal axis, CHORIO impacts EPO, MLT, SIRT1, and HIF signal transduction defined by dynamic changes in EPO, EPOR, MLTR1, SIRT1, HIF1α and HIF2α mRNA, and EPO protein. Notably, ligand-receptor mismatch, tissue compartment differential regulation, and non-receptor-mediated signaling highlight the importance, complexity and nuance of neural and immune cell development and provide essential clues to mechanisms of injury in PBI. As the placenta, immune cells, and neural cells share many common, developmentally regulated signal transduction pathways, further studies are needed to clarify the perinatal dynamics of EPO and MLT signaling and to capitalize on therapies that target endogenous neurorepair mechanisms.
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Alvarez, Mark, Bassem Skaff, Rawane El Assad, and Dani Zoorob. "Conservative Management of Iatrogenic Uterine Perforation at 22 Weeks of Gestation Permitting for a Third-Trimester Delivery." North American Proceedings in Gynecology & Obstetrics, June 28, 2024. http://dx.doi.org/10.54053/001c.121009.
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Introduction: Acute cholecystitis is one of the most common causes of nonobstetric procedures in pregnancy (Jayalal 2015; Post 2019; Tolcher 2018; Nezhat 1997), with suggested need for cholecystectomy if the diagnosis is made in pregnancy, irrespective of the indicators for urgent or emergent surgery (Post 2019). This is because delaying surgical treatment has been suggested as increasing the risk of perinatal morbidity and mortality (Jayalal 2015). Laparoscopic cholecystectomy in pregnancy can be safely performed, while recognizing the changes in anatomy and physiology occurring due to the ongoing conception (Jayalal 2015; Post 2019). However, inadvertent uterine perforation of the gravid uterus has been reported in the literature, resulting in risk of premature delivery, miscarriage, chorioamnionitis, and rupture (Tolcher 2018). In this report, we present a case of incidental iatrogenic second trimester uterine perforation by a trocar during laparoscopic cholecystectomy that was addressed conservatively following identification and repair which permitted for delay of delivery until early in the third-trimester delivery. Case Presentation: 32-year-old lady, G4P3 presented to the Emergency Department at 22+2/7 weeks of gestation with a two day history of epigastric pain, radiating to the right upper quadrant and the right shoulder. Surgical history was pertinent for one prior cesarean section due to breech presentation, with the uterine incision repaired in two layers. Vital signs were overall reassuring. The physical exam was consistent with a gravid uterus and a positive Murphy sign. Laboratory test results were significant for hyperglycemia: 207 (74-106mg/dl); SGOT: 78.2 (<31 UI/L); phosphatase alkaline: 235.4 (35-104 UI/L); lipase: 1524 (13-60 UI/L); and amylase: 781 (20-100 UI/L). Abdominal ultrasound showed a distended, thin-walled gallbladder containing several biliary stones of differing size with the common bile duct dilated at 0.4 cm. The patient was admitted for persistent abdominal pain refractory to analgesics. The general surgeon was consulted, and the plan was made for laparoscopic cholecystectomy upon reaching 23 weeks of gestation. Intraoperatively, three trocars were inserted and extensive adhesions were noted to invest the gallbladder, omentum, liver, and abdominal wall. A laceration measuring 1 cm in diameter in the uterine wall occurred with the introduction of the umbilical trocar as the uterus was adherent to the abdominal wall. The blind entry technique had been used. The trocar was mobilized and the adheiolysis performed. The cholecystectomy was successfully completed and upon reducing intrabdominal gas pressure, the amniotic fluid leak was noted. The general surgeon thereafter repaired the uterine laceration with a polyglactin suture in a figure of 8 fashion. Hemostasis was ensured. Postoperative obstetrical ultrasound performed soon thereafter suggested the presence of a 1000g fetus; cephalic presentation; fundal placenta with notable anterior and posterior uterine investment without signs of retroperitoneal hematoma or abruptio placentae. The amniotic fluid was suggested to be ‘cloudy’. The patient received a course of antibiotics and antenatal corticosteroids for postoperative chorioamnionitis prophylaxis and fetal lung maturity. She was also started on an oral progesterone. The patient was closely monitored with serial ultrasounds and fetal heart monitoring. At 28 weeks of gestation, the patient presented to the hospital with preterm labor at which time she received a second course of steroids for fetal lung maturity and was subsequently discharged after complete resolution of uterine contractions. One week later, the patient again developed episodic abdominal pain. Contraction tomography showed regular uterine contractions that was nonresponsive to conservative measures. She was then transferred to the operating room for urgent cesarean section due to concern of uterine rupture at the site of the injury. Cesarean intraoperative findings included a healing site where the uterine injury had occurred, with a near-complete dehiscence along the transverse axis of the lower transverse uterine segment. Examination of the placenta indicated trauma to the anterior uterine wall that had been of full thickness. Discussion: The incidence of cholecystitis in pregnancy ranges from 0.05% to 0.8% (Date 2008). The higher rates of incidence in pregnancy are due to expected physiologic changes, namely supersaturation of cholesterol driven by increased estrogen levels along with the relaxation of the smooth muscle in the gallbladder caused by elevated progesterone. Given these physiologic changes, risk of occurrence requiring admission has been reported to be as high as 38-70% after initial conservative treatment (Date 2008). The guidelines of the Japanese Society of Gastroenterological Endoscopic Surgery (published only in Japanese) recommend laparoscopic surgery during the second trimester (14-27 weeks) in pregnant women. In this report, we presented an unusual case of direct trocar injury at 23 weeks which was managed conservatively on outpatient basis with the injury site remaining intact despite a full wall thickness injury. This patient delivered via cesarean section at 29 weeks, after which the neonate remained inpatient in the NICU for a period of 2 months. This case demonstrates the utility of a conservative approach in the setting of a stable patient and fetus in the setting of an intrapartum iatrogenic uterine perforation. This is one of a few cases in published literature with successful neonatal outcomes. This approach opens the door for conservative management in future cases after weighing the potential risks of chorioamnionitis and uterine rupture which could develop at any time. Conclusion: While iatrogenic trocar injury in pregnancy is rare, conservative management and stabilization of the mother and fetus may be possible to delay delivery for steroid administration and promotion of fetal maturation. This case highlights the potential benefits of such management route in the setting of a stable pregnancy.