PMID- 29648494
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200525
IS  - 1607-8888 (Electronic)
IS  - 1025-3890 (Linking)
VI  - 21
IP  - 6
DP  - 2018 Nov
TI  - Placental glucocorticoid receptor and 11beta-hydroxysteroid dehydrogenase-2 
      recruitment indicates impact of prenatal adversity upon postnatal development in 
      mice.
PG  - 474-483
LID - 10.1080/10253890.2018.1460660 [doi]
AB  - Prenatal stress may increase concentrations of maternal glucocorticoids, which 
      restrict fetal growth, with variable impact upon postnatal development. Among key 
      regulators of stress hormone effects are the glucocorticoid receptor (GR) and 
      11beta-hydroxysteroid dehydrogenase-2 (11betaHSD2), the enzyme that inactivates 
      glucocorticoid. This study utilized mice selectively bred for social dominance 
      (Dom) or submissiveness (Sub), respectively exhibiting resilience or sensitivity 
      to stress, to test whether stress-induced alterations in placental GR and 11betaHSD2 
      protein expression may mediate divergent effects of prenatal adversity upon 
      postnatal development. Pregnant Dom and Sub dams underwent prenatal restraint 
      stress (PRS) for 45 min on gestational days (GD) 15-17. PRS induced a similar 
      spike in serum corticosterone concentrations of dams from each strain on GD15 
      (p < .001, n = 8), and impaired fetal growth (p < .01, n = 5 litters), although 
      Dom placentae were larger than Sub placentae (p < .01). Among placentae from Dom 
      dams, PRS elevated protein contents of both GR (p < .05, n = 5 litters) and 
      11betaHSD2 (p < .01) on GD19. In contrast, GR contents were reduced among placentae 
      from PRS-exposed Sub mice (p < .01), without changes in 11betaHSD2 content. 
      Correspondingly, Dom PRS pup growth recovered by PND14, yet Sub PRS pups remained 
      underweight into adolescence (p < .0001, n = 40 pups). Thus, prenatal stress more 
      strongly increased placental GR and 11betaHSD2 levels among Dom mice than in Subs. 
      Increased GR may improve placental function and up-regulate 11betaHSD2 expression, 
      protecting fetuses from effects of prenatal stress upon postnatal development. 
      Placental recruitment of GR and 11betaHSD2 are potential markers of stress-induced 
      developmental disorders, in accordance with maternal resilience or sensitivity to 
      stress.
FAU - Gross, Moshe
AU  - Gross M
AD  - Department of Molecular Biology, Ariel University, Ariel, Israel.
FAU - Romi, Hava
AU  - Romi H
AD  - Department of Molecular Biology, Ariel University, Ariel, Israel.
FAU - Gilimovich, Yelena
AU  - Gilimovich Y
AD  - Department of Molecular Biology, Ariel University, Ariel, Israel.
FAU - Drori, Elyashiv
AU  - Drori E
AD  - Department of Chemical Engineering and Biotechnology, Ariel University, Ariel, 
      Israel.
AD  - Agriculture and Oenology Research Department, Eastern R&D center, Ariel, Israel.
FAU - Pinhasov, Albert
AU  - Pinhasov A
AD  - Department of Molecular Biology, Ariel University, Ariel, Israel.
LA  - eng
PT  - Journal Article
DEP - 20180412
PL  - England
TA  - Stress
JT  - Stress (Amsterdam, Netherlands)
JID - 9617529
SB  - IM
OTO - NOTNLM
OT  - 11beta-Hydroxysteroid dehydrogenase-2 (11betaHSD2)
OT  - corticosterone
OT  - glucocorticoid receptor (GR)
OT  - placenta
OT  - postnatal development
OT  - prenatal restraint stress (PRS)
EDAT- 2018/04/13 06:00
MHDA- 2018/04/13 06:01
CRDT- 2018/04/13 06:00
PHST- 2018/04/13 06:00 [pubmed]
PHST- 2018/04/13 06:01 [medline]
PHST- 2018/04/13 06:00 [entrez]
AID - 10.1080/10253890.2018.1460660 [doi]
PST - ppublish
SO  - Stress. 2018 Nov;21(6):474-483. doi: 10.1080/10253890.2018.1460660. Epub 2018 Apr 
      12.