Ca2+ channel subunit a 1D inhibits endometriosis cell apoptosis and mediated by prostaglandin E2.

Abstract

Endometriosis is considered as a chronic pelvic inflammatory disease and prostaglandin E2(PGE2) (a kind of the inflammatory cytokines) was increased in the endometriosis patient's peritoneal fluid . Ca2+ signal and Ca2+ channels play an important role in cell apoptosis. This study was to explore the L-type calcium channel (Cav1.3) expression and its biological function in endometriosis. Furthermore the molecular mechanism between Cav1.3 and PGE2 was also clarified. The real-time PCR and immunohistochemical were used to detect the expression of Cav1.3. Apoptosis was detected by Flow cytometry assay and Western blot assay. Cav1.3 was high expression in endometriosis tissue and primary endometrial stromal cells (hEM15A). Treatment with PGE2 rapidly inhibited apoptosis and increased Cav1.3 expression in hEM15A . The silencing of Cav1.3 promoted apoptosis, which was unchanged after PGE2 treatment. Moreover, the inhibition of Cav1.3 by shRNA transfection activated cleaved PARP and cleaved caspase-3. These available evidences suggest that Cav1.3 is required for PGE2 induction apoptosis and relates to the pathophysiology of endometriosis. Interference with Cav1.3 may offer a neo-therapeutic window in endometriosis treatment.