Haoran Shen1, Yao Wang2. 1. Department of Gynecology, Obstetrics & Gynecology Hospital of Fudan University, Shanghai, P.R. China. 2. Department of Assisted Reproduction, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, P.R. China.
Abstract
OBJECTIVE: To investigate the role of the transforming growth factor-β1 (TGF-β1)/Smad3 signaling pathway in development of ovarian follicle by promoting apoptosis of granulosa cells in polycystic ovary syndrome (PCOS). METHODS: A total of 54 female rats were obtained and randomly assigned into the PCOS (n = 27) and control groups ( n = 27). PCOS rat models were constructed using the dehydroepi-androsterone method to observe ovarian morphology and ultrastructure. Chemiluminescence immunoassay was performed to detect the levels of luteinizing hormone, follicle stimulating hormone, estradiol, progesterone, and testosterone. The release of TGF-β1 in follicular fluid and serum was tested by the enzyme-linked immunosorbent assay. RESULTS: Expression of p-Smad3 significantly increased in granulosa cells of PCOS group. In terms of the Smad2 protein, there was no significant difference between the PCOS and control group. In comparison to the control group, the number of normal secondary follicles and normal antral follicles were significantly decreased, whereas the number of hypogenetic secondary follicles undergoing atresia and antral follicles were significantly elevated in the PCOS group. Furthermore, the thickness of granulosa cells decreased and the apoptosis of granulosa cells increased in the PCOS group compared with the control one. CONCLUSION: These results indicate that p-Smad3 may have a close relationship with apoptosis of granulosa cells, the mechanism is that the TGF-β1/Smad3 signaling pathway may inhibit development of ovarian follicle of PCOS by regulating the apoptosis of granulosa cells.
OBJECTIVE: To investigate the role of the transforming growth factor-β1 (TGF-β1)/Smad3 signaling pathway in development of ovarian follicle by promoting apoptosis of granulosa cells in polycystic ovary syndrome (PCOS). METHODS: A total of 54 female rats were obtained and randomly assigned into the PCOS (n = 27) and control groups ( n = 27). PCOSrat models were constructed using the dehydroepi-androsterone method to observe ovarian morphology and ultrastructure. Chemiluminescence immunoassay was performed to detect the levels of luteinizing hormone, follicle stimulating hormone, estradiol, progesterone, and testosterone. The release of TGF-β1 in follicular fluid and serum was tested by the enzyme-linked immunosorbent assay. RESULTS: Expression of p-Smad3 significantly increased in granulosa cells of PCOS group. In terms of the Smad2 protein, there was no significant difference between the PCOS and control group. In comparison to the control group, the number of normal secondary follicles and normal antral follicles were significantly decreased, whereas the number of hypogenetic secondary follicles undergoing atresia and antral follicles were significantly elevated in the PCOS group. Furthermore, the thickness of granulosa cells decreased and the apoptosis of granulosa cells increased in the PCOS group compared with the control one. CONCLUSION: These results indicate that p-Smad3 may have a close relationship with apoptosis of granulosa cells, the mechanism is that the TGF-β1/Smad3 signaling pathway may inhibit development of ovarian follicle of PCOS by regulating the apoptosis of granulosa cells.