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简介：AbstractServing as the interface between the fetal and maternal environments during gestation, the placenta plays critical roles in the protection of the developing fetus and the maintenance of maternal health. The placenta is primarily derived from the embryonic trophectoderm which differentiates into various subtypes of trophoblast cells through villous and extravillous pathways. The interactions among trophoblasts and multiple decidual cells and immune cells at the maternal-fetal interface fundamentally form the functional units of the placenta, which are responsible for blood perfusion and maternal-fetal material exchange, immune tolerance, and the regulation of pregnancy adaptation. Defects in placental development and functional maintenance are in tight association with adverse pregnancy outcomes such as preeclampsia. In this article, we review recent advances on human trophoblast cell differentiation and the construction of placental functional units and discuss the placental and maternal factors that may contribute to the occurrence of preeclampsia.

简介：AbstractObjective:To investigate the effects of vitrification on the expression of the imprinted gene Snrpn in neonatal placental tissue.Methods:Neonatal placental tissue was collected from women with natural pregnancy (control group) and from women in assisted reproductive technology (ART) pregnancy group, following fresh and vitrified embryo transfer (fresh group and vitrified group, respectively). Snrpn mRNA expression and SNRPN protein levels in placental tissue from these three groups were assessed by real-time reverse transcription polymerase chain reaction and Western blot, respectively. DNA methylation in the Snrpn promoter region was analyzed by bisulfite-pyrosequencing.Results:The expression of Snrpn mRNA and SNRPN protein was found to be higher in placental tissue from the fresh and vitrified ART groups, compared to the control group. There was no significant difference in SNRPN gene or protein expression between the fresh and vitrified groups. DNA methylation at the Snrpn promoter region was not significantly different between these three groups.Conclusions:Human ART may alter the transcriptional expression and protein levels of the imprinted gene Snrpn. However, compared to other ART methods, vitrification may not aggravate or reduce this effect. Moreover, the altered expression of Snrpn is likely not directly related to DNA methylation of the Snrpn promoter region.

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简介：BackgroundTherequisitetechniquesforsafefetalcardiacarrestduringcardiacinterventionsneedtobefurtherdeveloped.Furthermore,littleisknownaboutthepathophysiologiceffectofcardiopulmonarybypass(CPB)atdifferentlevelsoftemperaturewithcardioplegicarrestonthedevelopingfetus.MethodsTwelvepregnantgoatswererandomlydividedintohypothermicCPBgroup(Hgroup):cardiopulmonarybypasswithperfusionat30-32℃(n=6)andnormothermicCPBgroup(Ngroup):cardiopulmonarybypasswithperfusionat36℃-38℃(n=6).Fetalcardiopulmonarybypasswasmaintainedincluding30minutesofcardiacarrest.Fetalmeanarterialbloodpressure(MAP)andheartrate(HR)weremonitored.Fetalarterialbloodsampleswereanalyzed.Thepulseindex(PI)andresistanceindex(RI)ofthefetalumbilicalarterywererecorded.ResultsThematernalweight,fetalweightandpumpflowhadnosignificantdifferencebetweenthe2groups.Afterclampremoval,twofetalheartsdidnotauto-beatinHgroup.ThefetalHRandMAPbweresignificantlydifferent(P<0.05)etweenthe2groups.Therewasremarkabledecreasinginpost-CPBfetalHRandMAPinHgroup.AstabledecreaseinpartialpressureofoxygenwithaconcomitantstableincreaseofcarbondioxidepartialpressureinHgroupwasnoted.ThelacticacidinHgroupwassignificantlyhigherthanthatintheNgroup(P<0.05).ThePIandRIinHgroupweresignificantlyelevated1hourafteroffCPBandfurthermarkedlyincreased2hoursafteroffbypass.ConclusionsFetalCPBcouldbeperformedunderbothhypothermicandnormothermicconditions.However,normothermicbypassmayprovidebetterdeliveryofoxygentofetaltissue.

简介：AbstractObjective:Structural abnormalities and dysfunction of the placenta contribute to pregnancy-related complications, such as preeclampsia. Syncytin-A (synA) has been reported to be expressed in the placenta. The contribution of synA to developmental abnormalities and dysfunction of the placenta remains elusive. In this study, we aimed to explore the role of synA in placental development and functions.Methods:SynA-knockout mice were generated using the CRISPR-Cas9 method, and the phenotypes of the placenta and fetus of synA-knockout mice were observed. Real-time quantitative polymerase chain reaction (PCR) and routine PCR were employed to detect the genotypes of the offspring. CD31 immunohistochemistry was used to evaluate the vessel density of the placenta, and the protein levels of key molecules were measured by western blotting.Results:SynA knockout caused fetal death. Furthermore, synA-knockout mice showed placental developmental abnormalities, indicated by a thinner labyrinth layer, thicker spongiotrophoblast layer, lower blood vessel density, and significantly higher numbers of apoptotic trophoblasts, when compared with wild-type littermates. Mechanistically, synA ablation induced apoptosis-inducing factor (AIF) cleavage and nuclear localization and promoted placental trophoblast apoptosis. In addition, synA knockout increased the calpain1 protein levels. The calpain1 inhibitor calpeptin blocked synA knockout-induced AIF cleavage, partially restoring the placental structural abnormalities of synA-knockout mice.Conclusions:SynA knockout leads to placental developmental abnormalities by inducing trophoblastic apoptosis via the calpain1-AIF pathway.

简介：AbstractObjective:This study was aimed to determine the changes in CXCR2 expression in preeclampsia placenta and its correlation with clinical parameters.Methods:Sixty-four gravidas ranging in age from 25 to 42 years referred to the obstetrics unit of the West China Second University Hospital from April 2012 to October 2012 were recruited in this case-control study; women were diagnosed and divided into early-onset preeclampsia group (n= 22), late-onset preeclampsia group (n= 22), and healthy pregnancy group (n= 20). After immunolocalized in human placenta, the levels of CXCR2 protein and messenger ribonucleic acid (mRNA) were detected by enzyme-linked immunosorbent assay and real-time quantitative polymerase chain reaction. Correlations between placental CXCR2 protein expression with systolic blood pressure and lactate dehydrogenase (LDH) in early-onset preeclampsia were examined using Pearson or Spearman’s correlation coefficients.Results:Placental CXCR2 protein and mRNA expression in early-onset preeclampsia was significantly lower than it was in placentas from healthy pregnancy pregnancies and late-onset preeclampsia (P < 0.05). The placental CXCR2 protein expression correlated negatively with systolic blood pressure and LDH in early-onset preeclampsia (r= -0.51, P < 0.05; r=-0.43, P < 0.05).Conclusion:Significant abnormal placental CXCR2 expression in early-onset preeclampsia, and its correlations with some clinical parameters (systolic blood pressure and LDH) were discovered, suggesting that CXCR2 may play a role in the pathogenesis of early-onset preeclampsia.

简介：AbstractObjective:This study aimed at investigating the expression of nuclear factor kappa B (NF-κB) and mammalian target of rapamycin (mTOR) related signal pathways in liver tissues of intrahepatic cholestasis of pregnancy animal models.Methods:Estrogen (EE)-induced cholestasis and a placental ischemia-reperfusion (IR) model were established in pregnant rats. All pregnant rats were divided into four groups by random number table: EE-IR group (n= 6), EE-sham group (n = 6), control-IR group (n= 6) and control-sham group (n= 6). Liver expression of mTOR, its upstream regulator DNA damage response-1 (REDD1), and downstream factor glucose transporter type-1 (GLUT1), accompanied by NF-κB (p65 is the most important component), its activator toll-like receptor 4 (TLR4), and inhibitor IκBα, were detected by western blot analysis and real-time polymerase chain reaction. The intergroup comparisons were performed with a one-way analysis of variance, the comparisons among groups were analyzed with the nonparametric Kruskal-Wallis test.Results:Giving pregnant rats EE alone reduced the hepatic expression of IκBα (0.72 ± 0.20 vs. 1.01 ± 0.07, P= 0.008). Meanwhile, giving pregnant rats placental IR alone increased liver levels of REDD1 (3.24 ± 0.98 vs. 1.06 ± 0.24, P= 0.025), GLUT1 (2.37 ± 0.82 vs. 1.09 ± 0.10, P= 0.039), TLR4 (2.12 ± 0.29 vs. 1.20 ± 0.28, P= 0.010), and p65 (2.09 ± 0.85 vs. 1.04 ± 0.06, P= 0.023), and decreased hepatic mTOR (0.50 ± 0.07 vs. 1.01 ± 0.03, P= 0.001) and IκBα (0.61 ± 0.08 vs. 1.01 ± 0.07, P= 0.014) expression. Subjecting EE-treated rats to placental IR did not further alter liver levels of GLUT1 (2.02 ± 0.45 vs. 1.79 ± 0.39, P= 0.240), TLR4 (2.10 ± 0.74 vs. 1.60 ± 0.36, P= 0.129), or p65 (2.41 ± 0.83 vs. 1.65 ± 0.46, P= 0.145), whereas it did decrease hepatic mTOR (0.42 ± 0.09 vs. 0.90 ± 0.14, P= 0.008) and IκBα (0.43 ± 0.09 vs. 0.72 ± 0.20, P= 0.004) expression and enhance REDD1 expression (4.46 ± 0.65 vs. 2.05 ± 0.47, P= 0.009). Placental IR stress did impact the hepatic expression of REDD1-mTOR-GLUT1 and TLR4/NF-κB/IκBα in pregnant rats.Conclusion:Placental IR-induced hepatic GLUT1, TLR4, and p65 alternation, which responded efficiently in control rats, were impaired in EE-induced ICP rats.