GPER1 is required to protect fetal health from maternal inflammation.

Journal Article (Journal Article)

Type I interferon (IFN) signaling in fetal tissues causes developmental abnormalities and fetal demise. Although pathogens that infect fetal tissues can induce birth defects through the local production of type I IFN, it remains unknown why systemic IFN generated during maternal infections only rarely causes fetal developmental defects. Here, we report that activation of the guanine nucleotide-binding protein-coupled estrogen receptor 1 (GPER1) during pregnancy is both necessary and sufficient to suppress IFN signaling and does so disproportionately in reproductive and fetal tissues. Inactivation of GPER1 in mice halted fetal development and promoted fetal demise, but only in the context of maternal inflammation. Thus, GPER1 is a central regulator of IFN signaling during pregnancy that allows dynamic antiviral responses in maternal tissues while also preserving fetal health.

Full Text

Duke Authors

Cited Authors

  • Harding, AT; Goff, MA; Froggatt, HM; Lim, JK; Heaton, NS

Published Date

  • January 15, 2021

Published In

Volume / Issue

  • 371 / 6526

Start / End Page

  • 271 - 276

PubMed ID

  • 33446553

Pubmed Central ID

  • PMC8060949

Electronic International Standard Serial Number (EISSN)

  • 1095-9203

Digital Object Identifier (DOI)

  • 10.1126/science.aba9001


  • eng

Conference Location

  • United States