Recent reports have demonstrated that follicular atresia is initiated or caused by granulosa cell apoptosis followed by theca cell degeneration in mammalian ovaries, but the mechanism of follicular atresia is still to...Recent reports have demonstrated that follicular atresia is initiated or caused by granulosa cell apoptosis followed by theca cell degeneration in mammalian ovaries, but the mechanism of follicular atresia is still to be elucidated. Therefore, our present study was designed to examine our hypothesis that the changes of follicular microenvironment induce the granulosa cell apoptosis during pocrine follicular atresia in vivo. We firstly isolated intact porcine antral follicles and identified them into three groups, healthy follicles （HF）, early atretic follicles （EAF） and progressed atretic follicles （PAF） through morphology and histology. To further confirm their status, we detected hormone levels in follicular fluids and the expression level of apoptosis gene Bax in granulosa cells. The rate of progesterone （P） and estradiol （E2） was increased with the expression of Bax, indicating hormone can be used as a marker of granulosa cell apoptosis or follicular atresia. Finally, we analyzed the expression level of hormone receptor genes in granulosa cells and their relationship with follicular atresia. In PAF, the expression of Progesterone receptor （PGR） was increased significantly while estradiol receptor （ER） had no notable changes, which suggesting the increased-PGR accelerated the effect of P-stimulated granulosa cell apoptosis. The dramatic increasing of androgen receptor （AR） expression in PAF and the obvious increase of tumor necrosis factor-u receptor （TNFR） in EAF indicated that there are different pathways regulating granulosa cell apoptosis during follicular atresia. Together, our results suggested that different pathways of granulosa cell apoptosis was induced by changing the follicular microenvironment during follicular atresia.展开更多
Background The mechanisms of endometriosis with infertility have not been fully studied. The present study aimed to assess the follicular fluid （FF） levels of prostaglandin E2 （PGE2）, which plays a critical role w...Background The mechanisms of endometriosis with infertility have not been fully studied. The present study aimed to assess the follicular fluid （FF） levels of prostaglandin E2 （PGE2）, which plays a critical role within the ovary, and to investigate the effect of PGE2 on steroidogenesis in granulosa-lutein cells （GLCs） from women with and without endometriosis. Methods Thirty-three women with laparoscopically documented endometriosis and 40 controls undergoing in vitro fertilization （IVF） were studied. We assayed the concentrations of PGE2 in FF, the production of E2 and progesterone in FF and in culture medium, and the expression of steroidogenic acute regulatory protein （STAR） and CYP19A1 in GLCs with the intervention of PGE2. Results PGE2 and progesterone concentrations were increased and displayed positive correlation in endometriotic FE PGE2 induced the expression of STAR and the production of progesterone in GLCs from women with endometriosis, and the expression of STAR and the production of progesterone were increased in GLCs from women with endometriosis. However, there were no significant effects of PGE2 on promoting the production of E2 or the expression of CYP19A1 in GLCs. Moreover, the production of E2 and the expression of CYP19A1 in GLCs from women with endometriosis were significantly decreased compared to the controls. Conclusions PGE2 concentrations are increased in endometriotic FF, along with concomitant increases in progesterone and STAR. In contrast, the E2 and CYP19A1 are decreased in GLCs, which may delay the development of the follicles and cause an imbalance in the follicular steroid hormone levels. These changes may have close relationship with endometriosis-associated infertility.展开更多
基金supported by the National Basic Research Program of China (2007CB947403)the National Natural Science Foundation of China (31101705)the grant from Students Practice and Innovation Training Program of Jiangsu Province, China (JSS0909)
文摘Recent reports have demonstrated that follicular atresia is initiated or caused by granulosa cell apoptosis followed by theca cell degeneration in mammalian ovaries, but the mechanism of follicular atresia is still to be elucidated. Therefore, our present study was designed to examine our hypothesis that the changes of follicular microenvironment induce the granulosa cell apoptosis during pocrine follicular atresia in vivo. We firstly isolated intact porcine antral follicles and identified them into three groups, healthy follicles （HF）, early atretic follicles （EAF） and progressed atretic follicles （PAF） through morphology and histology. To further confirm their status, we detected hormone levels in follicular fluids and the expression level of apoptosis gene Bax in granulosa cells. The rate of progesterone （P） and estradiol （E2） was increased with the expression of Bax, indicating hormone can be used as a marker of granulosa cell apoptosis or follicular atresia. Finally, we analyzed the expression level of hormone receptor genes in granulosa cells and their relationship with follicular atresia. In PAF, the expression of Progesterone receptor （PGR） was increased significantly while estradiol receptor （ER） had no notable changes, which suggesting the increased-PGR accelerated the effect of P-stimulated granulosa cell apoptosis. The dramatic increasing of androgen receptor （AR） expression in PAF and the obvious increase of tumor necrosis factor-u receptor （TNFR） in EAF indicated that there are different pathways regulating granulosa cell apoptosis during follicular atresia. Together, our results suggested that different pathways of granulosa cell apoptosis was induced by changing the follicular microenvironment during follicular atresia.
文摘Background The mechanisms of endometriosis with infertility have not been fully studied. The present study aimed to assess the follicular fluid （FF） levels of prostaglandin E2 （PGE2）, which plays a critical role within the ovary, and to investigate the effect of PGE2 on steroidogenesis in granulosa-lutein cells （GLCs） from women with and without endometriosis. Methods Thirty-three women with laparoscopically documented endometriosis and 40 controls undergoing in vitro fertilization （IVF） were studied. We assayed the concentrations of PGE2 in FF, the production of E2 and progesterone in FF and in culture medium, and the expression of steroidogenic acute regulatory protein （STAR） and CYP19A1 in GLCs with the intervention of PGE2. Results PGE2 and progesterone concentrations were increased and displayed positive correlation in endometriotic FE PGE2 induced the expression of STAR and the production of progesterone in GLCs from women with endometriosis, and the expression of STAR and the production of progesterone were increased in GLCs from women with endometriosis. However, there were no significant effects of PGE2 on promoting the production of E2 or the expression of CYP19A1 in GLCs. Moreover, the production of E2 and the expression of CYP19A1 in GLCs from women with endometriosis were significantly decreased compared to the controls. Conclusions PGE2 concentrations are increased in endometriotic FF, along with concomitant increases in progesterone and STAR. In contrast, the E2 and CYP19A1 are decreased in GLCs, which may delay the development of the follicles and cause an imbalance in the follicular steroid hormone levels. These changes may have close relationship with endometriosis-associated infertility.
