| Literature DB >> 34099644 |
Diana Monsivais1,2, Takashi Nagashima3,4, Renata Prunskaite-Hyyryläinen5, Kaori Nozawa3,6, Keisuke Shimada7, Suni Tang3, Clark Hamor3, Julio E Agno3,6, Fengju Chen8, Ramya P Masand3, Steven L Young9, Chad J Creighton8,10, Francesco J DeMayo11, Masahito Ikawa7, Se-Jin Lee12,13, Martin M Matzuk14,15.
Abstract
During early pregnancy in the mouse, nidatory estrogen (E2) stimulates endometrial receptivity by activating a network of signaling pathways that is not yet fully characterized. Here, we report that bone morphogenetic proteins (BMPs) control endometrial receptivity via a conserved activin receptor type 2 A (ACVR2A) and SMAD1/5 signaling pathway. Mice were generated to contain single or double conditional deletion of SMAD1/5 and ACVR2A/ACVR2B receptors using progesterone receptor (PR)-cre. Female mice with SMAD1/5 deletion display endometrial defects that result in the development of cystic endometrial glands, a hyperproliferative endometrial epithelium during the window of implantation, and impaired apicobasal transformation that prevents embryo implantation and leads to infertility. Analysis of Acvr2a-PRcre and Acvr2b-PRcre pregnant mice determined that BMP signaling occurs via ACVR2A and that ACVR2B is dispensable during embryo implantation. Therefore, BMPs signal through a conserved endometrial ACVR2A/SMAD1/5 pathway that promotes endometrial receptivity during embryo implantation.Entities:
Year: 2021 PMID： 34099644 DOI： 10.1038/s41467-021-23571-5
Source DB: PubMed Journal: Nat Commun ISSN： 2041-1723 Impact factor: 14.919