p53 and Fas Are Sequential Mechanisms of Testicular Germ Cell Apoptosis

Wiley - Tập 23 Số 1 - Trang 64-70 - 2002
Yizhong Yin1, Brandon C. Stahl1, William C. DeWolf1, Abraham Morgentaler1
1Division of Urology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts

Tóm tắt

Testicular germ cell apoptosis in the cryptorchid testis is induced by abdominal heat stress. p53‐dependent apoptosis appears responsible for the initial phase of germ cell loss in experimental cryptorchidism based on a 3‐day delay of apoptosis in p53−1− mice. However, the mechanisms underlying the subsequent p53‐independent apoptosis have not been identified. Although studies have suggested that Fas plays a role in testicular germ cell apoptosis, no direct evidence has been shown. To test the hypothesis that Fas is involved in testicular germ cell apoptosis and is responsible for the p53‐independent phase of apoptosis in the cryptorchid testis, p53−1, Ipr/lpr (a spontaneous mutation in the Fas gene, which causes autoimmune disease) double‐mutant mice were generated and unilateral cryptorchidism was induced in these mice. It was found that testicular weight reduction and germ cell apoptosis were delayed by an additional 3 days, and the Fas production increased in the time frame of p53‐independent apoptosis in the experimental cryptorchid testis of wild‐type mice. These results suggest that Fas is involved in testicular germ cell apoptosis, and that Fas‐dependent apoptosis is responsible for the p53‐independent phase of germ cell apoptosis in the cryptorchid testis. The cascade of testicular germ cell apoptosis in response to heat stress implies the existence of sequential quality control mechanisms in spermatogenesis.

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Tài liệu tham khảo

10.1073/pnas.90.5.1756

Costabile RA, 1998, Cancer and male factor infertility, Oncology (Huntingt), 12, 557

10.1016/S0015-0282(16)43942-7

Fukui N., 1923, Action of body temperature on the testicle, Jpn Med World, 3, 160

10.1016/S0094-0143(05)70040-9

10.1016/S0960-9822(00)00002-6

Jensen TK, 1995, Do environmental estrogens contribute to the decline in male reproductive health?, Clin Chem, 41, 1896, 10.1093/clinchem/41.12.1896

10.1210/endo.140.2.6479

10.1210/endo.138.5.5110

10.1074/jbc.274.12.7756

10.1084/jem.188.11.2033

10.1095/biolreprod61.1.70

Nelson WO., 1951, Mammalian spermatogenesis: effect of experimental cryptorchidism in the rat and non-descent of the testis in man, Recent Prog Horm Res, 6, 29

O'Connor L, 2000, CD95 (Fas/APO-1) and p53 signal apoptosis independently in diverse cell types, Cancer Res, 60, 1217

10.1007/s002400050017

10.1159/000147881

10.1128/MCB.15.6.3032

10.1152/ajpendo.1999.276.2.E310

10.1016/S0378-4274(99)00253-2

10.1038/sj.cdd.4400490

10.1530/ror.0.0040038

10.1016/S0015-0282(16)33605-6

10.1095/biolreprod57.6.1267

VanDemark NL, 1970, The Testis, 233

10.1095/biolreprod60.2.461

10.1095/biolreprod58.2.492

10.1002/j.1939-4640.1997.tb01896.x

10.1210/en.140.7.3133

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Wiley

Tập 23 Số 1

64-70

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