Progesterone-regulated Hsd11b2 as a barrier to balance mouse uterine corticosterone
(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.
(Less)
- author
- Zheng, Zhan Hong ; Fu, Tao ; Zhang, Hai Yi ; Yang, Zhen Shan LU ; Zheng, Zhan Hong and Yang, Zeng Ming
- publishing date
- 2020-01
- 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}}, }