open access

Vol 90, No 12 (2019)
ORIGINAL PAPERS Gynecology
Published online: 2019-12-31
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Ca2+ channel subunit a 1D inhibits endometriosis cell apoptosis and mediated by prostaglandin E2

Yuan Yang, Yue Yuan, Xiaoling Ma, Fuling Xing
DOI: 10.5603/GP.2019.0115
·
Pubmed: 31909458
·
Ginekol Pol 2019;90(12):669-674.

open access

Vol 90, No 12 (2019)
ORIGINAL PAPERS Gynecology
Published online: 2019-12-31

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.

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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Keywords

endometriosis; Cav1.3; apoptosis; PGE2

About this article
Title

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

Journal

Ginekologia Polska

Issue

Vol 90, No 12 (2019)

Pages

669-674

Published online

2019-12-31

DOI

10.5603/GP.2019.0115

Pubmed

31909458

Bibliographic record

Ginekol Pol 2019;90(12):669-674.

Keywords

endometriosis
Cav1.3
apoptosis
PGE2

Authors

Yuan Yang
Yue Yuan
Xiaoling Ma
Fuling Xing

References (21)
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