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Interaction of insulin-like growth factor-binding protein-3 and BAX in mitochondria promotes male germ cell apoptosis

Yue Jia1, Kuk-Wha Lee, Ronald Swerdloff

  • 1Division of Endocrinology, Department of Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California 90509-2910, USA.

The Journal of Biological Chemistry
|November 6, 2009
PubMed

Insights

Insulin-like growth factor binding protein-3 (IGFBP-3) promotes male germ cell apoptosis by interacting with BAX, activating the mitochondria-dependent pathway. This novel pathway impacts male fertility and testicular disease.

Area of Science:

  • Reproductive Biology
  • Cell Biology
  • Endocrinology

Background:

  • Germ cell apoptosis is vital for spermatogenesis.
  • Intratesticular hormone deprivation can trigger germ cell apoptosis.

Purpose of the Study:

  • To investigate the role of insulin-like growth factor binding protein-3 (IGFBP-3) in male germ cell apoptosis.
  • To elucidate the mechanism of IGFBP-3-induced apoptosis.

Main Methods:

  • Adult Sprague-Dawley male rats were treated with saline, GnRH antagonist (GnRH-A), IGFBP-3, or a combination of GnRH-A and IGFBP-3.
  • Co-immunoprecipitation and enzyme-linked immunosorbent assays were used to assess IGFBP-3 and BAX interaction.
  • Release of cytochrome c and DIABLO from isolated testicular mitochondria was measured.

Main Results:

  • IGFBP-3 and GnRH-A treatments significantly increased germ cell apoptosis, with combined treatment showing further enhancement.
  • IGFBP-3 was found to associate with BAX in testicular mitochondria.
  • Both IGFBP-3 and BAX induced the release of cytochrome c and DIABLO from isolated mitochondria, with a synergistic effect observed when combined.

Conclusions:

  • IGFBP-3 interacts with BAX to activate germ cell apoptosis through the mitochondria-dependent pathway.
  • This novel pathway plays a role in regulating germ cell homeostasis.
  • The findings may have implications for male fertility and testicular diseases.

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