X-Message-Number: 12566
Date: Thu, 14 Oct 1999 22:16:50 -0700 (PDT)
From: Doug Skrecky <>
Subject: prolonging ovarian lifespan

Authors
  Perez GI.  Robles R.  Knudson CM.  Flaws JA.  Korsmeyer SJ.  Tilly JL.
Institution
  Vincent Center for Reproductive Biology, Massachusetts General Hospital and
  Department of Obstetrics, Gynecology and Reproductive Biology, Harvard
  Medical School, Boston 02114, USA.
Title
  Prolongation of ovarian
  lifespan into advanced chronological age by Bax-deficiency.
Source
  Nature Genetics.  21(2):200-3, 1999 Feb.
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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