Butyrate Improves Porcine Endometrial Epithelial Cell Receptivity via Enhancing Acetylation of Histone H3K9

ScopeUterine receptivity is a major restriction of embryo implantation and survival, and the endometrial luminal epithelium serves as the transient gateway for uterine receptivity and embryo implantation. Butyrate is reported to promote the success of embryo implantation, but the effects and mechanism of butyrate on uterine receptivity are still unknown. Methods and resultsPorcine endometrial epithelial cells (PEECs) are used as a model, and the cellular receptivity changes, metabolism, and gene expression profiles influenced by butyrate are analyzed. The study finds that butyrate improves receptive changes in PEECs, including inhibiting proliferation, exhibiting more pinocytosis on the cell surface, and increasing adhesiveness to porcine trophoblast cells. In addition, butyrate increases prostaglandin synthesis and markedly impacts purine metabolism, pyrimidine metabolism, and the FoxO signaling pathway. siRNA to inhibit the expression of FoxO1 and chromatin immunoprecipitation-sequencing (ChIP-seq) of H3K9ac are used to demonstrate that the H3K9ac/FoxO1/PCNA pathway can contribute to the effects of cell proliferation inhibition and uterine receptivity improvement induced by butyrate. ConclusionThe findings reveal that butyrate improves endometrial epithelial cell receptivity by enhancing the acetylation of histone H3K9, which shows nutritional regulation and therapeutic potential for poor uterine receptivity and difficulty in embryo implantation.

Automated summary

The study finds that butyrate improves endometrial epithelial cell receptivity by inhibiting cell proliferation, increasing pinocytosis activity on the cell surface, and enhancing adhesiveness to porcine trophoblast cells. Butyrate also increases prostaglandin synthesis and significantly affects purine metabolism, pyrimidine metabolism, and the FoxO signaling pathway. The H3K9ac/FoxO1/PCNA pathway is shown to contribute to the effects of cell proliferation inhibition and uterine receptivity improvement induced by butyrate through siRNA and ChIP-seq experiments.