4.2 Article

Hsc70 interacts with KCNA5 to promote the proliferation of granulosa cells in polycystic ovarian syndrome

Journal

TROPICAL JOURNAL OF PHARMACEUTICAL RESEARCH
Volume 21, Issue 4, Pages 693-699

Publisher

PHARMACOTHERAPY GROUP
DOI: 10.4314/tjpr.v21i4.2

Keywords

Hsc70; KCNA5; Granulosa cells; Polycystic ovary syndrome; Apoptosis

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The purpose of this study was to investigate the function and interaction of Hsc70 and KCNA5 in PCOS. The results showed that Hsc70 expression was upregulated in PCOS and overexpression of Hsc70 promoted granulosa cell proliferation while inhibiting apoptosis. KCNA5 expression was downregulated in PCOS and knockdown of KCNA5 promoted cell proliferation. Hsc70 promotes granulosa cell proliferation by interacting with KCNA5.
Purpose: To investigate the function and interaction of heat-shock cognate protein 70 (Hsc70) and potassium voltage-gated channel subfamily A member 5 (KCNA5) in polycystic ovary syndrome (PCOS). Methods: Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot were used to measure Hsc70 and KCNA5 expression in PCOS. The effect of Hsc70 on granulosa cell apoptosis was determined by flow cytometry. Cell counting kit-8 (CCK-8) and colony formation assay were used to assess the impact of Hsc70 on cell proliferation, while the interaction of Hsc70 with KCNA5 were evaluated by Western blot, CCK-8, and colony formation assay, respectively. Results: Hsc70 expression was upregulated in PCOS compared to the control (p < 0.05). In granulosa cells, Hsc70 overexpression promoted cell proliferation but inhibited apoptosis (p < 0.05), whereas Hsc70 knockdown suppressed cell proliferation and promoted apoptosis (p < 0.05). Furthermore, KCNA5 expression was downregulated in PCOS (p < 0.05) and was negatively correlated with Hsc70 expression. KCNA5 knockdown promoted granulosa cell proliferation and also attenuated the Hsc70 knockdown-mediated inhibition of granulosa cell proliferation (p < 0.05). Conclusion: Hsc70 promotes granulosa cell proliferation by interacting with KCNA5, further defining the molecular mechanism behind PCOS.

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