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

Author

Listed:
  • Diana Monsivais

    (Baylor College of Medicine
    Baylor College of Medicine)

  • Takashi Nagashima

    (Baylor College of Medicine
    Hanakoganei Ladies Clinic)

  • Renata Prunskaite-Hyyryläinen

    (University of Oulu)

  • Kaori Nozawa

    (Baylor College of Medicine
    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
    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
    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
    University of Connecticut School of Medicine, Department of Genetics and Genome Sciences)

  • Martin M. Matzuk

    (Baylor College of Medicine
    Baylor College of Medicine)

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.

Suggested Citation

  • 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 , 2021. "Endometrial receptivity and implantation require uterine BMP signaling through an ACVR2A-SMAD1/SMAD5 axis," Nature Communications, Nature, vol. 12(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-23571-5
    DOI: 10.1038/s41467-021-23571-5
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