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Ginekol Pol. 2019;90(12):669-674. doi: 10.5603/GP.2019.0115.

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

Author information

1
The Reproductive Medicine Special Hospital of the 1st hospital of Lanzhou University,Lanzhou,Gansu Province, No.1 Donggang road,chengguan distrct,lanzhou city,Gansu province, 730000 lanzhou, China.
2
Department of Obstetrics and Gynecology, Zhang ye Maternal And Child Health Care Hospital, China, China. recover0302@sina.com.

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.

KEYWORDS:

Cav1.3; PGE2; apoptosis; endometriosis

PMID:
31909458
DOI:
10.5603/GP.2019.0115
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