Testis

Follicle-Stimulating Hormone Affects Spermatogonial Survival by Regulating the Intrinsic Apoptotic Pathway in Adult Rats

Abstract
FSH plays a key role in spermatogonial development in adult rats via poorly understood mechanisms. We aimed to identify the role of this hormone in the regulation of germ cell apoptosis and proliferation in adult rats by suppression of FSH action following passive immunoneutralization with a rat FSH antibody for 4 and 7 days. Apoptosis and proliferation were identified by TUNEL and PCNA labelling methods, respectively. Intrinsic and extrinsic apoptotic pathways were identified by immunohistochemistry, stereological techniques and RT PCR by assessing pathway-specific proteins and genes. Following FSH suppression for 4 and 7 days, we have previously reported a 30% decrease in spermatogonial number, with an increased apoptosis in a stage-specific manner. The present study also shows stage specific increases in apoptosis with no changes in proliferation. This increase in apoptosis was attributable to an increase in spermatogonial apoptosis via the intrinsic, rather than extrinsic pathway, as shown by increased activated caspase 9 positive spermatogonia. The concomitant suppression of FSH and LH/T showed that T alone or together with FSH was more important in spermatocyte and spermatid survival by regulating both apoptotic pathways. A reduction in the level of the intrinsic pathway transcript Bcl2l2 (apoptosis suppressor gene) following FSH suppression for 4 days shows that FSH regulates some components of the intrinsic pathway. This study reveals that FSH predominantly acts as a survival factor for spermatogonia by regulating the intrinsic pathway, while having no affect of germ cell proliferation in rats in vivo.

Key words: Mechanisms of Hormone Action • Testis • Apoptosis • Follicle-stimulating hormone • Spermatogenesis

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