Caspase-independent death of meiotic and postmeiotic cells overexpressing p53: calpain involvement

Male 0301 basic medicine Cell Death Calpain Caspase 3 Molecular Sequence Data Caspase 2 Gene Expression Mice, Transgenic Spermatids Caspase 9 Gene Expression Regulation, Enzymologic Enzyme Activation Meiosis Mice 03 medical and health sciences Caspases Animals Amino Acid Sequence RNA, Messenger Sequence Alignment Infertility, Male
DOI: 10.1038/sj.cdd.4401887 Publication Date: 2006-03-10T10:13:35Z
ABSTRACT
In a model of male sterility (MTp53) owing to enforced p53 expression in spermatocytes II and spermatids of transgenic mice, we focused on the role of caspases. Most of them are expressed in all differentiation stages, but only the transcriptional levels of caspase-2 and caspase-3 are modified in MTp53 germ cells. In normal testis, cleaved caspase-3 and caspase-9 are detected during the elongation of spermatids. Despite this constitutive presence of caspases during terminal differentiation, calpains are the main effectors of germ cell loss in MTp53 testes: calpain 1 RNA levels are increased, caspase-3-like activity is markedly decreased while calpain activity is higher and the calpain inhibitor E64d ((2S, 3S)-trans-epoxysuccinyl-L-leucylamido-3-methylbutane ethyl ester) reduces TUNEL labeling in MTp53 testis, whereas pancaspase inhibitor zVADfmk (N-benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone) has no effect. Our work suggests that despite the presence, and potent involvement, of caspases in male haploid cell maturation, calpains are the executioners of the death of terminally differentiating germ cells.
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