z-logo
open-access-imgOpen Access
miR-200 Regulates Endometrial Development During Early Pregnancy
Author(s) -
Patricia T. Jimenez,
Monica Mainigi,
R. Ann Word,
W. Lee Kraus,
Carole R. Mendelson
Publication year - 2016
Publication title -
molecular endocrinology
Language(s) - English
Resource type - Journals
eISSN - 1944-9917
pISSN - 0888-8809
DOI - 10.1210/me.2016-1050
Subject(s) - decidualization , biology , stromal cell , gene knockdown , decidual cells , endometrium , embryo , decidua , endocrinology , microbiology and biotechnology , medicine , microrna , homeobox , andrology , cancer research , pregnancy , fetus , transcription factor , placenta , cell culture , gene , genetics
For successful embryo implantation, endometrial stromal cells must undergo functional and morphological changes, referred to as decidualization. However, the molecular mechanisms that regulate implantation and decidualization are not well defined. Here we demonstrate that the estradiol- and progesterone-regulated microRNA (miR)-200 family was markedly down-regulated in mouse endometrial stromal cells prior to implantation, whereas zinc finger E-box binding homeobox-1 and -2 and other known and predicted targets were up-regulated. Conversely, miR-200 was up-regulated during in vitro decidualization of human endometrial stromal cells. Knockdown of miR-200 negatively affected decidualization and prevented the mesenchymal-epithelial transition-like changes that accompanied decidual differentiation. Notably, superovulation of mice and humans altered miR-200 expression. Our findings suggest that hormonal alterations that accompany superovulation may negatively impact endometrial development and decidualization by causing aberrant miR-200 expression.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom