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Prenatal exposure to dexamethasone disturbs sex-determining gene expression and fetal testosterone production in male embryos.

Authors
 Hyo Jung Yun  ;  Ji-Yeon Lee  ;  Myoung Hee Kim 
Citation
 BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.471(1) : 149-155, 2016 
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
ISSN
 0006-291X 
Issue Date
2016
MeSH
Animals ; Anti-Inflammatory Agents/poisoning ; Dexamethasone/poisoning* ; Female ; Fetus/drug effects ; Fetus/physiopathology* ; Gene Expression Regulation, Developmental/drug effects* ; Male ; Mice ; Mice, Inbred ICR ; Pregnancy ; Prenatal Exposure Delayed Effects/metabolism* ; Sex Characteristics ; Sex Differentiation/drug effects* ; Testis/drug effects ; Testis/embryology ; Testis/metabolism ; Testosterone/biosynthesis*
Keywords
Dexamethasone ; Glucocorticoid ; Prenatal stress ; Sex-determining genes ; Testosterone
Abstract
Prenatal stress is known to cause intrauterine fetal growth retardation, and is also associated with various long-term effects in the form of metabolic and neurodevelopmental diseases in adults. Many of the diseases associated with prenatal stress exhibit a sex bias. Perturbations and vulnerability to prenatal stress are often more profound in males, but the mechanisms responsible for this relationship are not clear. We have previously shown that administration of the synthetic glucocorticoid, dexamethasone (Dex), at embryonic days 7.5, 8.5, and 9.5, induces embryonic growth restriction in a sex-dependent manner in a mouse model. Here we examined the effect of prenatal exposure to Dex on gonadal development. During male gonadal development, sex-determining genes, such as Sry, Sox9, and other downstream genes, were found to be dysregulated in response to prenatal Dex, whereas the genes for the ovarian pathway were affected to a lesser degree in females. In addition, fetal testosterone concentrations were decreased by prenatal exposure to Dex, in parallel with reduced numbers of 3β-hydroxysteroid dehydrogenase (3β-HSD)-positive cells in the embryonic testis. These results show that prenatal exposure to Dex differentially influences male versus female on the gene expression and hormone production during sex determination. We believe these studies provide valuable insights into possible mechanisms responsible for sex-specific responses to prenatal stress.
Full Text
http://www.sciencedirect.com/science/article/pii/S0006291X16301619
DOI
10.1016/j.bbrc.2016.01.161
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Anatomy (해부학교실) > 1. Journal Papers
Yonsei Authors
Kim, Myoung Hee(김명희) ORCID logo https://orcid.org/0000-0001-5652-1452
Lee, Ji Yeon(이지연) ORCID logo https://orcid.org/0000-0002-0670-3095
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/146456
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