| Title: |
GPER1 is required to protect fetal health from maternal inflammation |
| Authors: |
Harding, Alfred T.; Goff, Marisa A.; Froggatt, Heather M.; Lim, Jean K.; Heaton, Nicholas S. |
| Contributors: |
National Heart, Lung, and Blood Institute; National Cancer Institute; National Institute of Allergy and Infectious Diseases; The Hartwell Foundation |
| Source: |
Science ; volume 371, issue 6526, page 271-276 ; ISSN 0036-8075 1095-9203 |
| Publisher Information: |
American Association for the Advancement of Science (AAAS) |
| Publication Year: |
2021 |
| Description: |
GPER1 in utero to the rescue! Several common pathogens, including influenza A virus (IAV), can activate systemic type I interferon (IFN) signaling during pregnancy. Such infections would be expected to cause birth defects and fetal mortality, but maternal IAV infections rarely produce such effects, suggesting the presence of a protective mechanism in fetal tissues. Harding et al. used a CRISPR screen to uncover IFN regulators that can mediate differential IFN control across tissues in human cell lines. They found that G protein–coupled estrogen receptor 1 (GPER1), which is expressed in fetal tissues, acts as a protective suppressor of IFN responses in the placenta during maternal infection. In a mouse model, pharmacological activation of GPER1 shielded fetuses from maternal inflammation. Activation of GPER1 might be promising therapeutically to protect the fetus from both maternal and fetal infections. Science , this issue p. 271 |
| Document Type: |
article in journal/newspaper |
| Language: |
English |
| DOI: |
10.1126/science.aba9001 |
| Availability: |
https://doi.org/10.1126/science.aba9001; https://syndication.highwire.org/content/doi/10.1126/science.aba9001; https://www.science.org/doi/pdf/10.1126/science.aba9001 |
| Accession Number: |
edsbas.312694BA |
| Database: |
BASE |