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Akt1 suppresses radiation-induced germ cell apoptosis in vivo

Teresa Rasoulpour1, Kathryn DiPalma, Branko Kolvek

  • 1Department of Pathology and Laboratory Medicine, Brown University, Providence, Rhode Island 02912, USA.

Endocrinology
|June 10, 2006
PubMed

Insights

The serine-threonine kinase Akt1 protects male germ cells from radiation damage. Akt1-deficient mice show increased apoptosis and sensitivity in spermatogonia after ionizing radiation exposure.

Area of Science:

  • Reproductive Biology
  • Molecular Biology
  • Radiation Biology

Background:

  • Radiation exposure is a known cause of germ cell injury, leading to apoptosis.
  • The Akt1 kinase pathway is involved in cell survival against various stressors.
  • The role of Akt1 in testicular radiation injury in vivo was previously unexplored.

Purpose of the Study:

  • To investigate the protective role of Akt1 in the testis following radiation-induced germ cell injury.
  • To determine the sensitivity of germ cells to radiation in Akt1-deficient mice.

Main Methods:

  • Examined apoptosis incidence in Akt1-deficient mice after ionizing radiation exposure.
  • Assessed Akt kinase activity in testes of wild-type mice post-irradiation.
  • Analyzed mRNA and protein expression of Akt isoforms (Akt1, Akt2, Akt3).

Main Results:

  • Akt kinase activity increased in wild-type mouse testes after ionizing radiation.
  • Loss of Akt1 led to earlier onset of germ cell apoptosis and increased sensitivity of mitotic spermatogonia.
  • Akt2 and Akt3 expression were not induced in Akt1-deficient mice.

Conclusions:

  • Akt1 plays a crucial role in germ cell survival after radiation-induced testicular injury.
  • Akt2 also contributes to germ cell survival, though to a lesser extent than Akt1.
  • Fas ligand may be involved in regulating the response to testicular radiation injury.

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