Regulation of spermatogenic cell apoptosis by the pro-apoptotic proteins in the testicular tissues of mammalian and avian species.

Apoptosis of germ cells is an important feature of spermatogenesis, as this process allows the removal of excess germ cells from testicular tissue. This is crucial to control the number of germ cells that can be supported and nourished by the Sertoli cells. It has been established that up to 75 % of germ cells are lost during the development of spermatogonia. In this process, germ cells with defective genes are removed. Also, apoptosis regulates homeostasis of testicular tissue by maintaining a balance between germ cell proliferation and cell death. This is necessary as it guarantees normal spermatogenesis. Apoptosis also occurs during maturation divisions of spermatocytes and spermatids but albeit to a lesser extent. Several factors, known pro-apoptotic proteins, play a critical role in the process of apoptosis. The most vital pro-apoptotic proteins are caspase-3, B-cells lymphoma 2 (Bcl2), truncated BH3 interacting death domain (tBID), tumor suppressor protein (p53), and Bcl-2 associated protein (BAX). Execution of apoptosis may be triggered by either an extrinsic or an intrinsic pathway. The extrinsic pathway is initiated by death receptors and death ligands. Death receptors trigger pro-apoptotic proteins such as caspase-3 for the execution of apoptosis. The intrinsic pathway, on the other hand, is triggered by nutrient deprivation, stress, or DNA damage, which in turn activates Bcl2 families of pro-apoptotic proteins that foster apoptosis. The present review focuses on pro-apoptotic proteins and their mechanisms of action, with special emphasis on their involvement in germ cell apoptosis in the testicular tissues of mammalian and avian species.
Competing Interests: Declaration of Competing Interest The authors declare that there are no competing interests.
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