Endometrial receptivity and implantation require uterine BMP signaling through an ACVR2A-SMAD1/SMAD5 axis

Diana Monsivais (), Takashi Nagashima, Renata Prunskaite-Hyyryläinen, Kaori Nozawa, Keisuke Shimada, Suni Tang, Clark Hamor, Julio E. Agno, Fengju Chen, Ramya P. Masand, Steven L. Young, Chad J. Creighton, Francesco J. DeMayo, Masahito Ikawa, Se-Jin Lee and Martin M. Matzuk ()
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Diana Monsivais: Baylor College of Medicine
Takashi Nagashima: Baylor College of Medicine
Renata Prunskaite-Hyyryläinen: University of Oulu
Kaori Nozawa: Baylor College of Medicine
Keisuke Shimada: Osaka University
Suni Tang: Baylor College of Medicine
Clark Hamor: Baylor College of Medicine
Julio E. Agno: Baylor College of Medicine
Fengju Chen: Baylor College of Medicine
Ramya P. Masand: Baylor College of Medicine
Steven L. Young: University of North Carolina
Chad J. Creighton: Baylor College of Medicine
Francesco J. DeMayo: National Institute of Environmental Health Sciences
Masahito Ikawa: Osaka University
Se-Jin Lee: Jackson Laboratory for Genomic Medicine
Martin M. Matzuk: Baylor College of Medicine

Nature Communications, 2021, vol. 12, issue 1, 1-17

Abstract: 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.

Date: 2021
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DOI: 10.1038/s41467-021-23571-5

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