GPER1 is required to protect fetal health from maternal inflammation

doi:10.1126/science.aba9001

GSTDTAP > 气候变化

DOI	10.1126/science.aba9001
	GPER1 is required to protect fetal health from maternal inflammation
	Alfred T. Harding; Marisa A. Goff; Heather M. Froggatt; Jean K. Lim; Nicholas S. Heaton
	2021-01-15
发表期刊	Science
出版年	2021
英文摘要	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][1] 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. [1]: /lookup/doi/10.1126/science.aba9001
领域	气候变化 ; 资源环境
URL	查看原文
引用统计
文献类型	期刊论文
条目标识符	http://119.78.100.173/C666/handle/2XK7JSWQ/311500
专题	气候变化资源环境科学
推荐引用方式 GB/T 7714	Alfred T. Harding,Marisa A. Goff,Heather M. Froggatt,et al. GPER1 is required to protect fetal health from maternal inflammation[J]. Science,2021.
APA	Alfred T. Harding,Marisa A. Goff,Heather M. Froggatt,Jean K. Lim,&Nicholas S. Heaton.(2021).GPER1 is required to protect fetal health from maternal inflammation.Science.
MLA	Alfred T. Harding,et al."GPER1 is required to protect fetal health from maternal inflammation".Science (2021).