Follicular Growth and Atresia in Mammalian Ovaries : Regulation by Survival and Death of Granulosa Cells

Access this Article

Author(s)

    • INOUE Naoko INOUE Naoko
    • Laboratory or Animal Morphology and Function, Graduate School of Bioagricultural Sciences, Nagoya University
    • MANABE Noboru [他] MANABE Noboru
    • Research Unit for Animal Life Sciences, Animal Resource Science Center, Graduate School of Agricultural and Life Sciences, The University of Tokyo
    • OHKURA Satoshi
    • Laboratory of Animal Production Science, Graduate School of Bioagricultural Sciences, Nagoya University

Abstract

The mammalian ovary is an extremely dynamic organ in which a large majority of follicles are effectively eliminated throughout their reproductive life. Due to the numerous efforts of researchers, mechanisms regulating follicular growth and atresia in mammalian ovaries have been clarified, not only their systemic regulation by hormones (gonadotropins) but also their intraovarian regulation by gonadal steroids, growth factors, cytokines and intracellular proteins. Granulosa cells in particular have been demonstrated to play a major role in deciding the fate of follicles, serving molecules that are essential for follicular growth and maintenance as well as killing themselves by an apoptotic process that results in follicular atresia. In this review, we discuss the factors that govern follicular growth and atresia, with a special focus on their regulation by granulosa cells. First, ovarian folliculogenesis in adult life is outlined. Then, we explain about the regulation of follicular growth and atresia by granulosa cells, in which hormones, growth factors and cytokines, death ligand-receptor system and B cell lymphoma/leukemia 2 (BCL2) family members (mitochondria-mediated apoptosis) are further discussed.

Journal

  • Journal of Reproduction and Development

    Journal of Reproduction and Development 58(1), 44-50, 2012-02-01

    THE SOCIETY FOR REPRODUCTION AND DEVELOPMENT

References:  96

Codes

  • NII Article ID (NAID)
    10030407021
  • NII NACSIS-CAT ID (NCID)
    AA10936678
  • Text Lang
    ENG
  • Article Type
    REV
  • ISSN
    09168818
  • NDL Article ID
    023510652
  • NDL Call No.
    Z54-H305
  • Data Source
    CJP  NDL  J-STAGE 
Page Top