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      Prolongation of ovarian lifespan into advanced chronological age by Bax-deficiency

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          Abstract

          Female mammals are endowed with a finite number of oocytes at birth, each enclosed by a single layer of somatic (granulosa) cells in a primordial follicle. The fate of most follicles is atretic degeneration, a process that culminates in near exhaustion of the oocyte reserve at approximately the fifth decade of life in women, leading to menopause. Apoptosis has a fundamental role in follicular atresia, and recent studies have shown that Bax, which is expressed in both granulosa cells and oocytes, may be central to ovarian cell death. Here we show that young adult female Bax-/- mice possess threefold more primordial follicles in their ovarian reserve than their wild-type sisters, and this surfeit of follicles is maintained in advanced chronological age, such that 20-22-month-old female Bax-/- mice possess hundreds of follicles at all developmental stages and exhibit ovarian steroid-driven uterine hypertrophy. These observations contrast with the ovarian and uterine atrophy seen in aged wild-type female mice. Aged female Bax-/- mice fail to become pregnant when housed with young adult males; however, metaphase II oocytes can be retrieved from, and corpora lutea form in, ovaries of aged Bax-/- females following superovulation with exogenous gonadotropins, and some oocytes are competent for in vitro fertilization and early embryogenesis. Therefore, ovarian lifespan can be extended by selectively disrupting Bax function, but other aspects of normal reproductive performance remain defective in aged Bax-/- female mice.

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          Most cited references14

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          Regulation of ovarian follicular development in primates: facts and hypotheses.

          A Gougeon (1996)
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            A Quantitative and Cytological Study of Germ Cells in Human Ovaries

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              Apoptosis and ovarian function.

              J Tilly (1996)
              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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                Author and article information

                Journal
                Nature Genetics
                Nat Genet
                Springer Science and Business Media LLC
                1061-4036
                1546-1718
                February 1999
                February 1999
                : 21
                : 2
                : 200-203
                Article
                10.1038/5985
                9988273
                afd33c23-0359-4cb2-b3b2-a961e692f221
                © 1999

                http://www.springer.com/tdm

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