美国杜克大学医学院Nicholas S. Heaton研究组发现，GPER1能够保护胎儿免受母体炎症的影响。相关论文于2021年1月15日发表于国际学术期刊《科学》。

研究人员发现，鸟嘌呤核苷酸结合蛋白偶联雌激素受体1（GPER1）的激活在怀孕期间既是抑制I型干扰素（IFN）信号的必要条件，又是充分抑制因子，并且其在生殖和胎儿组织中的抑制作用不成比例。小鼠中GPER1的失活终止了胎儿的发育并促进了胎儿的死亡，但这仅发生在母体发炎的情况下。因此，GPER1是妊娠期间IFN信号传导的核心调节因子，可在母体组织中产生动态抗病毒反应，同时还能保持胎儿健康。

据介绍，胎儿组织中的IFN信号会导致发育异常和胎儿死亡。尽管感染胎儿组织的病原体可以通过局部产生I型IFN来诱发出生缺陷，但仍不清楚为什么在孕产妇感染期间产生的全身性IFN很少会引起胎儿发育缺陷。

附：英文原文

Title: GPER1 is required to protect fetal health from maternal inflammation

Author: Alfred T. Harding, Marisa A. Goff, Heather M. Froggatt, Jean K. Lim, Nicholas S. Heaton

Issue&Volume: 2021/01/15

Abstract: 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.

DOI: 10.1126/science.aba9001

Source: https://science.sciencemag.org/content/371/6526/271