PMID- 35378222
OWN - NLM
STAT- MEDLINE
DCOM- 20220525
LR  - 20220613
IS  - 1873-1708 (Electronic)
IS  - 0890-6238 (Linking)
VI  - 110
DP  - 2022 Jun
TI  - Effects of prenatal hypoxia on placental glucocorticoid barrier: Mechanistic 
      insight from experiments in rats.
PG  - 78-84
LID - S0890-6238(22)00048-X [pii]
LID - 10.1016/j.reprotox.2022.03.016 [doi]
AB  - Prenatal hypoxia is the most common stress in mid-late gestation that usually 
      arise from maternal, placental and/or fetal factors. As a multifunctional organ 
      enabling optimal fetal growth, placenta must adapt to diverse environmental 
      stressors. Excessive glucocorticoids exposure is known to have adverse effects on 
      fetal growth. The fetus is shielded by a placental glucocorticoid barrier by 
      11beta-hydroxysteroid dehydrogenase 2 (11beta-HSD2). However, the effects and 
      underlying mechanisms of intrauterine hypoxia on placental glucocorticoid barrier 
      are largely unknown. This study was the first to determine the effects and its 
      mechanisms. Pregnant rats were exposed to hypoxia (10.5% O2) from gestational day 
      (GD)10-20. At GD20, expression of 11-betaHSD2 were determined in placenta, and 
      corticosterone levels were measured in maternal and fetal plasma. Prenatal 
      hypoxia disrupted the placental glucocorticoid barrier by suppressing 11-betaHSD2 
      expression. Meanwhile, the decreased 11-betaHSD2 was correlated with an increased 
      DNA methylation within its gene promoter. Together, these results indicated that 
      prenatal hypoxia impair placental glucocorticoid barrier, was strongly associated 
      with reprogrammed 11-betaHSD2 expression via a DNA methylation-mediated epigenetic 
      mechanism.
CI  - Copyright (c) 2022 Elsevier Inc. All rights reserved.
FAU - Ji, Bingyu
AU  - Ji B
AD  - Institute for Fetology, First Hospital of Soochow University, Suzhou 215006, PR 
      China.
FAU - Lei, Jiahui
AU  - Lei J
AD  - Institute for Fetology, First Hospital of Soochow University, Suzhou 215006, PR 
      China.
FAU - Xu, Ting
AU  - Xu T
AD  - Institute for Fetology, First Hospital of Soochow University, Suzhou 215006, PR 
      China.
FAU - Zhao, Meng
AU  - Zhao M
AD  - Institute for Fetology, First Hospital of Soochow University, Suzhou 215006, PR 
      China.
FAU - Cai, Honghong
AU  - Cai H
AD  - Gynaecology and Obstetrics, First Hospital of Soochow University, Suzhou 215006, 
      PR China.
FAU - Qiu, Junlan
AU  - Qiu J
AD  - Department of Oncology and Hematology, Affiliated Suzhou Science and Technology 
      Town Hospital of Nanjing Medical University, Suzhou, China. Electronic address: 
      qiujunland@163.com.
FAU - Gao, Qinqin
AU  - Gao Q
AD  - Institute for Fetology, First Hospital of Soochow University, Suzhou 215006, PR 
      China. Electronic address: jennyqgao@126.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20220401
PL  - United States
TA  - Reprod Toxicol
JT  - Reproductive toxicology (Elmsford, N.Y.)
JID - 8803591
RN  - 0 (Glucocorticoids)
RN  - EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenase Type 2)
SB  - IM
MH  - 11-beta-Hydroxysteroid Dehydrogenase Type 2/genetics/metabolism
MH  - Animals
MH  - DNA Methylation
MH  - Female
MH  - *Glucocorticoids/toxicity
MH  - Hypoxia/metabolism
MH  - *Placenta/metabolism
MH  - Pregnancy
MH  - Rats
OTO - NOTNLM
OT  - 11-betaHSD2
OT  - DNA methylation
OT  - Placental glucocorticoid barrier
OT  - Prenatal hypoxia
EDAT- 2022/04/05 06:00
MHDA- 2022/05/26 06:00
CRDT- 2022/04/04 20:10
PHST- 2022/01/10 00:00 [received]
PHST- 2022/03/25 00:00 [revised]
PHST- 2022/03/29 00:00 [accepted]
PHST- 2022/04/05 06:00 [pubmed]
PHST- 2022/05/26 06:00 [medline]
PHST- 2022/04/04 20:10 [entrez]
AID - S0890-6238(22)00048-X [pii]
AID - 10.1016/j.reprotox.2022.03.016 [doi]
PST - ppublish
SO  - Reprod Toxicol. 2022 Jun;110:78-84. doi: 10.1016/j.reprotox.2022.03.016. Epub 
      2022 Apr 1.