Hypoxia-hindered methylation of PTGIS in endometrial stromal cells accelerates endometriosis progression by inducing CD16^- NK-cell differentiation.

ABSTRACT: Prostacyclin (PGI₂) plays key roles in shaping the immune microenvironment and modulating vasodilation, whereas its contribution to endometriosis (EMs) remains largely unclear. Our study suggested that prostacyclin synthase (PTGIS)-dependent PGI₂ signaling was significantly activated in EMs, which was involved in the hypoxic microenvironment of ectopic lesions and deficient methylation status of the PTGIS promoter. Notably, in vitro assays, hypoxia promoted PTGIS expression through DNA methyltransferase 1 (DNMT1)-mediated DNA methylation deficiency in endometrial stromal cells (ESCs); PTGIS overexpression enhanced the adhesive ability of ESCs and led to elevated PGI₂ production, and PGI₂ triggered CD16^- (encoded by FCGR3, Fc fragment o

SUBMITTER: Peng H 

PROVIDER: S-EPMC9356144 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature