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

Yuan Yang, Yue Yuan, Xiaoling Ma, Fuling Xing
Ginekologia polska · 2019 · vol. 90(12) , pp. 669–674 · doi:10.5603/gp.2019.0115 · PMID:31909458 · W2997671179
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Abstract

OBJECTIVES: 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. MATERIAL AND METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

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mesh:D004715endometriosis

MeSH descriptors

Calcium Channels, L-Type Dinoprostone Endometriosis Endometriosis Endometriosis Endometriosis Apoptosis Apoptosis Calcium Channels, L-Type Cells, Cultured Dinoprostone Female Humans Immunohistochemistry Ovary Ovary Signal Transduction Signal Transduction Stromal Cells Stromal Cells

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