Back to Search
Start Over
Caspase-2 involvement during ionizing radiation-induced oocyte death in the mouse ovary.
- Source :
-
Cell death and differentiation [Cell Death Differ] 2007 Apr; Vol. 14 (4), pp. 671-81. Date of Electronic Publication: 2006 Nov 03. - Publication Year :
- 2007
-
Abstract
- In mammals, the pool of primordial follicles at birth is determinant for female fertility. Exposure to IR during oogonia proliferation and the diplotene stages of ovarian development induced the virtual disappearance of primordial follicles in the postnatal ovary, while half the follicular reserve remained present after irradiation during the zygotene/pachytene stages. This sensitivity difference was correlated with the level of caspase-2 expression evaluated by immunohistochemistry. At the diplotene stage, Western blot and caspase activity analysis revealed that caspase-2 was activated 2 h after irradiation and a significant increase in the number of oocytes expressing cleaved caspase-9 and -3 occurred 6 h after treatment. Inhibition of caspase-2 activity prevented the cleavage of caspase-9 and partially prevented the loss of oocytes in response to irradiation. Taken together, our results show that caspase-2-dependent activation of the mitochondrial apoptotic pathway is one of the mechanisms involved in the genotoxic stress-induced depletion of the primordial follicle pool.
- Subjects :
- Animals
Apoptosis physiology
Enzyme Activation
Enzyme Inhibitors pharmacology
Female
Fertility radiation effects
Fetus enzymology
Gene Regulatory Networks genetics
Gene Regulatory Networks radiation effects
Humans
Immunohistochemistry
Mice
Mice, Inbred Strains
Oocytes enzymology
Ovary embryology
Ovary enzymology
Pregnancy
Apoptosis radiation effects
Caspase 2 metabolism
Fetus radiation effects
Oocytes radiation effects
Ovary radiation effects
Subjects
Details
- Language :
- English
- ISSN :
- 1350-9047
- Volume :
- 14
- Issue :
- 4
- Database :
- MEDLINE
- Journal :
- Cell death and differentiation
- Publication Type :
- Academic Journal
- Accession number :
- 17082817
- Full Text :
- https://doi.org/10.1038/sj.cdd.4402052