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Progesterone-regulated Hsd11b2 as a barrier to balance mouse uterine corticosterone

Zheng, Zhan Hong ; Fu, Tao ; Zhang, Hai Yi ; Yang, Zhen Shan LU orcid ; Zheng, Zhan Hong and Yang, Zeng Ming (2020) In Journal of Endocrinology 244(1). p.177-187
Abstract

Glucocorticoids (GCs) are essential for mouse embryo implantation and decidualization. Excess GCs are harmful for mouse embryo implantation and decidualization. 11β-Hydroxysteroid dehydrogenases type I and II (Hsd11b1/Hsd11b2) are main enzymes for regulating local level of GCs. Hsd11b2 acts as the placental glucocorticoid barrier to protect the fetus from excessive exposure. Although effects of GCs on the fetus and placenta in late pregnancy have been extensively studied, the effects of these adrenal corticosteroids in early pregnancy are far less well defined. Therefore, we examined the expression, regulation and function of Hsd11b1/Hsd11b2 in mouse uterus during early pregnancy. We found that Hsd11b2 is highly expressed in endometrial... (More)

Glucocorticoids (GCs) are essential for mouse embryo implantation and decidualization. Excess GCs are harmful for mouse embryo implantation and decidualization. 11β-Hydroxysteroid dehydrogenases type I and II (Hsd11b1/Hsd11b2) are main enzymes for regulating local level of GCs. Hsd11b2 acts as the placental glucocorticoid barrier to protect the fetus from excessive exposure. Although effects of GCs on the fetus and placenta in late pregnancy have been extensively studied, the effects of these adrenal corticosteroids in early pregnancy are far less well defined. Therefore, we examined the expression, regulation and function of Hsd11b1/Hsd11b2 in mouse uterus during early pregnancy. We found that Hsd11b2 is highly expressed in endometrial stromal cells on days 3 and 4 of pregnancy and mainly upregulated by progesterone (P4). In both ovariectomized mice and cultured stromal cells, P4 significantly stimulates Hsd11b2 expression. P4 stimulation of Hsd11b2 is mainly mediated by the Ihh pathway. The uterine level of corticosterone (Cort) is regulated by Hsd11b2 during preimplantation. Embryo development and the number of inner cell mass cells are suppressed by Cort treatment. These results indicate that P4 should provide a low Cort environment for the development of preimplantation mouse embryos by promoting the expression of uterine Hsd11b2.

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author
; ; ; ; and
publishing date
type
Contribution to journal
publication status
published
keywords
Corticosterone, Endometrium, Glucocorticoid barrier, Hsd11b2, Progesterone
in
Journal of Endocrinology
volume
244
issue
1
pages
177 - 187
publisher
Society for Endocrinology
external identifiers
  • pmid:31600723
  • scopus:85075812454
ISSN
0022-0795
DOI
10.1530/JOE-19-0349
language
English
LU publication?
no
additional info
Funding Information: This work was supported by National Key Research and Development Program of China (2018YFC1004403) and National Natural Science Foundation of China (31471397, 31272263 and 31671563). Funding Information: Program of China (2018YFC1004403) and National Natural Science Foundation of China (31471397, 31272263 and 31671563). Funding Information: This work was supported by National Key Research and Development Publisher Copyright: © 2020 Society for Endocrinology Published by Bioscientifica Ltd. Printed in Great Britain
id
d85f92c1-a67c-47ba-8480-96f50ae439d1
date added to LUP
2024-02-28 15:08:52
date last changed
2024-03-16 15:35:58
@article{d85f92c1-a67c-47ba-8480-96f50ae439d1,
  abstract     = {{<p>Glucocorticoids (GCs) are essential for mouse embryo implantation and decidualization. Excess GCs are harmful for mouse embryo implantation and decidualization. 11β-Hydroxysteroid dehydrogenases type I and II (Hsd11b1/Hsd11b2) are main enzymes for regulating local level of GCs. Hsd11b2 acts as the placental glucocorticoid barrier to protect the fetus from excessive exposure. Although effects of GCs on the fetus and placenta in late pregnancy have been extensively studied, the effects of these adrenal corticosteroids in early pregnancy are far less well defined. Therefore, we examined the expression, regulation and function of Hsd11b1/Hsd11b2 in mouse uterus during early pregnancy. We found that Hsd11b2 is highly expressed in endometrial stromal cells on days 3 and 4 of pregnancy and mainly upregulated by progesterone (P4). In both ovariectomized mice and cultured stromal cells, P4 significantly stimulates Hsd11b2 expression. P4 stimulation of Hsd11b2 is mainly mediated by the Ihh pathway. The uterine level of corticosterone (Cort) is regulated by Hsd11b2 during preimplantation. Embryo development and the number of inner cell mass cells are suppressed by Cort treatment. These results indicate that P4 should provide a low Cort environment for the development of preimplantation mouse embryos by promoting the expression of uterine Hsd11b2.</p>}},
  author       = {{Zheng, Zhan Hong and Fu, Tao and Zhang, Hai Yi and Yang, Zhen Shan and Zheng, Zhan Hong and Yang, Zeng Ming}},
  issn         = {{0022-0795}},
  keywords     = {{Corticosterone; Endometrium; Glucocorticoid barrier; Hsd11b2; Progesterone}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{177--187}},
  publisher    = {{Society for Endocrinology}},
  series       = {{Journal of Endocrinology}},
  title        = {{Progesterone-regulated Hsd11b2 as a barrier to balance mouse uterine corticosterone}},
  url          = {{http://dx.doi.org/10.1530/JOE-19-0349}},
  doi          = {{10.1530/JOE-19-0349}},
  volume       = {{244}},
  year         = {{2020}},
}