Bid and Bax Are Involved in Granulosa Cell Apoptosis During Follicular Atresia in Porcine Ovaries

Access this Article

Author(s)

Abstract

More than 99% of follicles undergo "atresia" during follicular development and growth. Follicular atresia is predominantly regulated by granulosa cell apoptosis. However, the intracellular signaling pathway of apoptosis in granulosa cells has not been revealed. In the present study, we examined changes in the expression of BH3-interacting domain death agonist (Bid) and Bcl-2-associated X protein (Bax), which are considered to promote the cell death ligand/receptor-mediated process in mitochondrion-dependent type II apoptosis, in porcine granulosa cells during atresia. Levels of mRNA and protein of Bid and Bax were determined by the reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting techniques, respectively. Levels of Bid and Bax mRNA and protein were markedly increased in granulosa cells of early atretic follicles compared with those of healthy follicles. <i>In situ</i> hybridization and immunohistochemical staining revealed that mRNA and protein of Bid and Bax were present in the granulosa cells, though only traces were found in healthy follicles; however, strong staining was noted in atretic follicles. These results indicate that Bid and Bax appear to be signal transduction factors in granulosa cells during follicular atresia and appear to play proapoptotic roles and confirm that the porcine granulosa cell is a mitochondrion-dependent type II apoptotic cell.<br>

Journal

  • Journal of Reproduction and Development

    Journal of Reproduction and Development 57(3), 421-427, 2011-06-01

    THE SOCIETY FOR REPRODUCTION AND DEVELOPMENT

References:  55

Cited by:  3

Codes

  • NII Article ID (NAID)
    10029050858
  • NII NACSIS-CAT ID (NCID)
    AA10936678
  • Text Lang
    ENG
  • Article Type
    Journal Article
  • ISSN
    09168818
  • NDL Article ID
    11132007
  • NDL Source Classification
    ZR22(科学技術--農林水産--畜産)
  • NDL Call No.
    Z54-H305
  • Data Source
    CJP  CJPref  NDL  J-STAGE 
Page Top