Survival and Apoptotic Signaling Pathways in Ovarian Follicle and Oocyte Development

Endocrine, cytokine and growth factors act in an autocrine and paracrine mechanisms for follicle and oocyte development. Current focus is on knowing how these activating and inhibiting factors act on primordial follicle to undergo transition from primary follicle to oocyte maturation. During oocyte development, due to LH stimulation, ligand of GPR3 is inactivated leading to inactivation of Gs subunit of GPR3 and in turn activation of Gi subunit of GPR3 by GTPase-activating proteins (GAPs). Gi which in turn inactivates Adenyl cyclase (AC) leads to meiotic resumption. Rise in Ca2+ level following LH stimulation also inhibits AC and activates phosphodiesterase (PDE) in turn leading to oocyte maturation. Apoptosis is essential for ovary function and development. Apoptosis loss includes quality control to eliminate meiotic anomalies. Only less than 1% of ovarian follicles which are present at birth will complete their path to ovulate. In fetal life oocyte generally undergo apoptosis, in adult life granulosa cell undergo apoptosis. These events are governed by prosurvival and pro-apoptotic factors. The equilibrium between these two factors (prosurvival molecules like Bcl-2, Bcl-x, TRAIL, TVB and the pro-apoptotic molecules like Bax, Bok, Bad, and Bak) may contribute to the regulation of ovarian follicle and oocyte apoptosis. Identification of these factors or patterns of expressions may contribute to the knowledge of mechanisms of growth of healthy oocytes with full developmental competence.