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For decades, the mechanisms responsible for germ cell depletion from the ovary, either directly during the perinatal period or indirectly via follicular atresia during postnatal life, have remained relatively obscure. The recent application of sensitive biochemical techniques for the study of cell death to the analysis of ovarian function has revealed that these two events, as well as a third instance of ovarian cell degeneration (luteolysis), are dependent upon the activation of physiological cell death mechanisms. It is therefore hypothesized that the controlled deletion of ovarian cell populations is accomplished via activation of a 'universal' pathway of cellular suicide involving altered expression of a conserved cohort of genes. The identity of the hormonal and intracellular effectors responsible for the coordination of life and death decisions made by ovarian cells during development as well as the biological and clinical implications of gene-directed cell death in the ovary are explored in this review.
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K. Hosokawa, D. Aharoni, A. Dantes, E. Shaulian, C. Schere-Levy, R. Atzmon, F. Kotsuji, M. Oren, I. Vlodavsky, and A. Amsterdam Modulation of Mdm2 Expression and p53-Induced Apoptosis in Immortalized Human Ovarian Granulosa Cells Endocrinology, November 1, 1998; 139(11): 4688 - 4700. [Abstract] [Full Text] [PDF] |
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L. Bergeron, G. I. Perez, G. Macdonald, L. Shi, Y. Sun, A. Jurisicova, S. Varmuza, K. E. Latham, J. A. Flaws, J. C.M. Salter, et al. Defects in regulation of apoptosis in caspase-2-deficient mice Genes & Dev., May 1, 1998; 12(9): 1304 - 1314. [Abstract] [Full Text] |
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J. Li, J.-M. Kim, P. Liston, M. Li, T. Miyazaki, A. E. Mackenzie, R. G. Korneluk, and B. K. Tsang Expression of Inhibitor of Apoptosis Proteins (IAPs) in Rat Granulosa Cells during Ovarian Follicular Development and Atresia Endocrinology, March 1, 1998; 139(3): 1321 - 1328. [Abstract] [Full Text] [PDF] |
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F. Otsuka, S. Yamamoto, G. F. Erickson, and S. Shimasaki Bone Morphogenetic Protein-15 Inhibits Follicle-stimulating Hormone (FSH) Action by Suppressing FSH Receptor Expression J. Biol. Chem., March 30, 2001; 276(14): 11387 - 11392. [Abstract] [Full Text] [PDF] |
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