scholarly journals Seasonally variant gene expression in full‐term human placenta

2020 ◽  
Vol 34 (8) ◽  
pp. 10431-10442
Author(s):  
Danielle A. Clarkson‐Townsend ◽  
Elizabeth Kennedy ◽  
Todd M. Everson ◽  
Maya A. Deyssenroth ◽  
Amber A. Burt ◽  
...  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tsung-Po Lai ◽  
Mark Simpson ◽  
Krunal Patel ◽  
Simon Verhulst ◽  
Jungsik Noh ◽  
...  

AbstractRecent hypotheses propose that the human placenta and chorioamniotic membranes (CAMs) experience telomere length (TL)-mediated senescence. These hypotheses are based on mean TL (mTL) measurements, but replicative senescence is triggered by short and dysfunctional telomeres, not mTL. We measured short telomeres by a vanguard method, the Telomere shortest length assay, and telomere-dysfunction-induced DNA damage foci (TIF) in placentas and CAMs between 18-week gestation and at full-term. Both the placenta and CAMs showed a buildup of short telomeres and TIFs, but not shortening of mTL from 18-weeks to full-term. In the placenta, TIFs correlated with short telomeres but not mTL. CAMs of preterm birth pregnancies with intra-amniotic infection showed shorter mTL and increased proportions of short telomeres. We conclude that the placenta and probably the CAMs undergo TL-mediated replicative aging. Further research is warranted whether TL-mediated replicative aging plays a role in all preterm births.


2020 ◽  
Vol 87 (9) ◽  
pp. S292
Author(s):  
Patricia Pehme ◽  
Kaitlin Carson ◽  
Wei Zhang ◽  
Valentina Nikulina ◽  
Yoko Nomura

PLoS ONE ◽  
2010 ◽  
Vol 5 (6) ◽  
pp. e10947 ◽  
Author(s):  
Joana Carvalho Moreira de Mello ◽  
Érica Sara Souza de Araújo ◽  
Raquel Stabellini ◽  
Ana Maria Fraga ◽  
Jorge Estefano Santana de Souza ◽  
...  

Placenta ◽  
2010 ◽  
Vol 31 (8) ◽  
pp. 698-704 ◽  
Author(s):  
K.J. Lee ◽  
S.H. Shim ◽  
K.M. Kang ◽  
J.H. Kang ◽  
D.Y. Park ◽  
...  

2018 ◽  
Vol 33 (11) ◽  
pp. 1123-1134 ◽  
Author(s):  
Woong Kim ◽  
Yoon Cho ◽  
Mi-Kyung Song ◽  
Jung-hee Lim ◽  
Jin young Kim ◽  
...  

2006 ◽  
Vol 290 (1) ◽  
pp. C305-C312 ◽  
Author(s):  
M. Desforges ◽  
H. A. Lacey ◽  
J. D. Glazier ◽  
S. L. Greenwood ◽  
K. J. Mynett ◽  
...  

The system A amino acid transporter is encoded by three members of the Slc38 gene family, giving rise to three subtypes: Na+-coupled neutral amino acid transporter (SNAT)1, SNAT2, and SNAT4. SNAT2 is expressed ubiquitously in mammalian tissues; SNAT1 is predominantly expressed in heart, brain, and placenta; and SNAT4 is reported to be expressed solely by the liver. In the placenta, system A has an essential role in the supply of neutral amino acids needed for fetal growth. In the present study, we examined expression and localization of SNAT1, SNAT2, and SNAT4 in human placenta during gestation. Real-time quantitative PCR was used to examine steady-state levels of system A subtype mRNA in early (6–10 wk) and late (10–13 wk) first-trimester and full-term (38–40 wk) placentas. We detected mRNA for all three isoforms from early gestation onward. There were no differences in SNAT1 and SNAT2 mRNA expression with gestation. However, SNAT4 mRNA expression was significantly higher early in the first trimester compared with the full-term placenta ( P < 0.01). We next investigated SNAT4 protein expression in human placenta. In contrast to the observation for gene expression, Western blot analysis revealed that SNAT4 protein expression was significantly higher at term compared with the first trimester ( P < 0.05). Immunohistochemistry and Western blot analysis showed that SNAT4 is localized to the microvillous and basal plasma membranes of the syncytiotrophoblast, suggesting a role for this isoform of system A in amino acid transport across the placenta. This study therefore provides the first evidence of SNAT4 mRNA and protein expression in the human placenta, both at the first trimester and at full term.


PLoS ONE ◽  
2016 ◽  
Vol 11 (1) ◽  
pp. e0147013 ◽  
Author(s):  
Ximi K. Wang ◽  
Monica Agarwal ◽  
Nataliya Parobchak ◽  
Alex Rosen ◽  
Anna M. Vetrano ◽  
...  

2003 ◽  
Vol 47 (1) ◽  
pp. 109-116 ◽  
Author(s):  
Xiaohong Zhang ◽  
Takashi Nakaoka ◽  
Toshihide Nishishita ◽  
Nobukazu Watanabe ◽  
Koichi Igura ◽  
...  

2018 ◽  
Vol 103 (4) ◽  
pp. 1545-1557 ◽  
Author(s):  
Sruthi Alahari ◽  
Martin Post ◽  
Alessandro Rolfo ◽  
Rosanna Weksberg ◽  
Isabella Caniggia

Abstract Context The von Hippel Lindau (VHL) protein is a key executor of the cellular hypoxic response that is compromised in preeclampsia, a serious disorder complicating 5% to 7% of pregnancies. To date, the mechanisms controlling VHL gene expression in the human placenta remain elusive. Objective We examined VHL epigenetic regulation in normal pregnancy and in preeclampsia, a pathology characterized by placental hypoxia. Design, Setting, and Participants Placentae were obtained from early-onset preeclampsia (n = 56; &lt;34 weeks of gestation) and late-onset preeclampsia (n = 19; ≥34 weeks of gestation). Placentae from healthy normotensive age-matched preterm control (n = 43) and term control (n = 23) pregnancies were included as controls. Main Outcome Measure(s) We measured the activity of Jumonji domain containing protein 6 (JMJD6), a ferrous iron (Fe2+)– and oxygen-dependent histone demethylase, and examined its function in the epigenetic control of VHL. Results JMJD6 regulates VHL gene expression in the human placenta. VHL downregulation in preeclampsia is dependent on decreased JMJD6 demethylase activity due to hypoxia and reduced Fe2+ bioavailability. Chromatin immunoprecipitation assays revealed decreased association of JMJD6 and its histone targets with the VHL promoter. Findings in preeclampsia were corroborated in a murine model of pharmacological hypoxia using FG-4592. Placentae from FG-4592–treated mice exhibited reduced VHL levels, accompanied by placental morphological alterations and reduced pup weights. Notably, Fe2+ supplementation rescued JMJD6 histone demethylase activity in histone from E-PE and FG-4592–treated mice. Conclusions Our study uncovers epigenetic regulation of VHL and its functional consequences for altered oxygen and iron homeostasis in preeclampsia.


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