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

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