Trophoblastic signals facilitate endometrial interferon response and lipid metabolism, ensuring normal decidualization

作者：Ningjie Yang, Yang Sun, Bing Han, Na Deng, Gaizhen Li, Qian Han, Yinan Wang, Han Cai, Fan Liu, Bin Cao, Wenbo Deng, Haili Bao, Shuangbo Kong, Jinhua Lu, Haibin Wang · 发表于：Cell Reports · 年份：2024 · DOI：10.1016/j.celrep.2024.114246 · 被引用次数：11 · 研究领域：Reproductive System and Pregnancy、Pregnancy and preeclampsia studies、Endometriosis Research and Treatment

The decidua plays a crucial role in providing structural and trophic support to the developing conceptus before placentation. Following embryo attachment, embryonic components intimately interact with the decidual tissue. While evidence indicates the participation of embryo-derived factors in crosstalk with the uterus, the extent of their impact on post-implantation decidual development requires further investigation. Here, we utilize transgenic mouse models to selectively eliminate primary trophoblast giant cells (pTGCs), the embryonic cells that interface with maternal tissue at the forefront. pTGC ablation impairs decidualization and compromises decidual interferon response and lipid metabolism. Mechanistically, pTGCs release factors such as interferon kappa (IFNK) to strengthen the decidual interferon response and lipoprotein lipase (LPL) to enhance lipid accumulation within the decidua, thereby promoting decidualization. This study presents genetic and metabolomic evidence reinforcing the proactive role of pTGC-derived factors in mobilizing maternal resources to strengthen decidualization, facilitating the normal progression of early pregnancy.