Heat shock protein 10 regulated apoptosis of mouse ovarian granulosa cells英文文献.pdfVIP

Gynecological Endocrinology, 2010; Early Online, 1–8 Heat shock protein 10 regulated apoptosis of mouse ovarian granulosa cells 1 1 1 2 3 1 1 1 JING LING , KAOKAO ZHAO , YU-GUI CUI , YING LI , XINRU WANG , MEI LI , KAI XUE , XIANG MA , JIA-YIN LIU 1 1 2 Center of Clinical Reproductive Medicine, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China, Jiangsu Province Family Planning Institute, Nanjing 210036, China, and 3Department of Public Health, Nanjing Medical University, Nanjing 210029, China (Received 23 October 2009; revised 28 February 2010; accepted 15 March 2010) Abstract 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 50.05. Knock- down of HSP10 in mouse GCs significantly increased apoptosis (p 50.05), whereas overexpression of HSP10