Effects Of Several Reproductive Hormones On Apoptosis Of Ovarian Granulose Cells Of Yaks In Vitro

The vast majority of follicles undergo a degenerative process in reproductive I ife. Apoptotic eel I death is the fundamental mechanism in response to follicular atresia. Moreover, the apoptosis of granulose cells (GCs) is implicated in directly mediating atretic process. Multiple studies have confirmed that the apoptotic process of GCs is not only related to apoptotic genes, but triggered by cytokines related to reproduction and Caspases family. Cell adhesion and extra cellular matrix in follicles also play an important intraovarian role. Importantly, the reproductive hormones have strongly related to control ovarian GCs apoptosis. Immense evidence implied that hormones as modulators may integrate into a network modulating apoptosis of granulose cells. However, the frame of the network has not been well outlined yet. Therefore, the present study is aimed at acquiring new evidence for the network by defining the effects of melatcnin (Mel), gonadotropin-releasing hormone (GnRH), fol I icular-st imulat ing hormone (FSH), leiteininzing hormone(LH), estrodiol-17 P (E2) and progesterone (P? on apoptosis, proliferation and differentiation in vitro in GCsobtained from large preovulatory follicles of yaks in nature estrus, us i ng f I ow cytometry and HE h i stochem i ca I assay to i nvest i gate apoptot i c incidence and proliferation index of GCs, and radioimmunoassay to evaluate the concentrations of progesterone and estrogen in culture med i a, and e I ectron and I i ght m i croscopes methods to observe and conf i rm cellar structure. The results showed that the granulose cells could produce progesterone and estrogen in vitro. Trends in proliferation of GCs treated by FSH, Mel, P< and LH were evident. FSH, Mel, P4 and E2 could I ead to the suppress i on of an i ntr i ns i c apoptos i s of GCs; FSH had stronger role in the suppression than other three hormones, and the effects couldn' t be affected by GnRH and Mel. The effect of Mel on apoptosis of GCs could be easi ly affected by the co-treatments with GnRH, FSH, LH, P4 and E2, but no addition effects was found with each other. GnRH could significantly induce the apoptosis of cultured GCs in vitro, whi le the apoptosis in response to GnRH could be completely inverted by FSH co-treatment and part i a II y decreased by Me I, E2 and P4 co-treatments. FSH, Mel, LH and E2 could increase the production of progesterone of cultured GCs in vitro respectively, and there is an addition effect of Mel and E2 on progesterone product ion. GnRH could mar Red I y suppress progesterone secretion of cultured GCs with or without FSH and LH co-treatments. E2 could invert the suppression of GnRH completely, also had the additive action on secreting progesterone with GnRH co-treatment. Mel partial ly released the suppression action of GnRH. FSH, LH, Mel, GnRH and P4 could s i gn i f icant I y promote GCs secret i ng estrogen i n v itro. Mel cou Id i nhi b it the action of P4 on GCs secreting estrogen. Co-treatments of GnRH and FSH or LH could decrease the activity of estrogen secretion.