Atrial natriuretic peptide promotes uterine decidualization and TRAIL expression in endometrial stromal cells, leading to sequential smooth muscle cell death and endothelial cell apoptosis.
ANP plays a critical role in pregnancy by promoting uterine decidualization and a TRAIL-dependent mechanism for spiral artery remodeling.
Atrial natriuretic peptide (ANP) is an important hormone in cardiovascular biology. It is activated by the protease corin. In pregnancy, ANP and corin promote uterine spiral artery remodeling, but the underlying mechanism remains unknown. Here we report an ANP function in uterine decidualization and TNF-related apoptosis-inducing ligand-dependent (TRAIL-dependent) death in spiral arterial smooth muscle cells (SMCs) and endothelial cells (ECs). In ANP- or corin-deficient mice, uterine decidualization markers and TRAIL expression were decreased, whereas in cultured human endometrial stromal cells (HESCs), ANP increased decidualization and TRAIL expression. In uterine spiral arteries from pregnant wild-type mice, SMC and EC loss occurred sequentially before trophoblast invasion. In culture, TRAIL from decidualized HESCs induced apoptosis in uterine SMCs, but not in ECs with low TRAIL receptor expression. Subsequently, cyclophilin B was identified from apoptotic SMCs that upregulated endothelial TRAIL receptor and caused apoptosis in ECs. These results indicate that ANP promotes decidualization and TRAIL expression in endometrial stromal cells, contributing to sequential events in remodeling of spiral arteries, including SMC death and cyclophilin B release, which in turn induces TRAIL receptor expression and apoptosis in ECs.
Zhang et al. (Thu,) conducted a other in Pregnancy / Uterine spiral artery remodeling. Atrial natriuretic peptide (ANP) vs. ANP- or corin-deficient models was evaluated on Uterine decidualization markers, TRAIL expression, and apoptosis in spiral arterial smooth muscle cells and endothelial cells. Atrial natriuretic peptide promotes uterine decidualization and TRAIL expression in endometrial stromal cells, leading to sequential smooth muscle cell death and endothelial cell apoptosis.