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Key apoptotic pathways for heat-induced programmed germ cell death in the testis.

Authors: Hikim, AP  Lue, Y  Yamamoto, CM  Vera, Y  Rodriguez, S  Yen, PH  Soeng, K  Wang, C  Swerdloff, RS 
Citation: Hikim AP, etal., Endocrinology. 2003 Jul;144(7):3167-75.
Pubmed: (View Article at PubMed) PMID:12810573
DOI: Full-text: DOI:10.1210/en.2003-0175

Short-term exposure (43 C for 15 min) of the rat testis to mild heat results within 6 h in stage- and cell-specific activation of germ cell apoptosis. Initiation of apoptosis was preceded by a redistribution of Bax from a cytoplasmic to paranuclear localization in heat-susceptible germ cells. Here we show that the relocation of Bax is accompanied by cytosolic translocation of cytochrome c and is associated with activation of the initiator caspase 9 and the executioner caspases 3, 6, and 7 and cleavage of poly(ADP) ribose polymerase. Furthermore, early in apoptosis, a significant amount of Bax also accumulates in endoplasmic reticulum, as assessed by Western blot analyses of fractionated testicular lysates. In additional studies using the FasL-defective gld mice, we have shown that heat-induced germ cell apoptosis is not blocked, thus providing evidence that the Fas signaling system may be dispensable for heat-induced germ cell apoptosis in the testis. Taken together, these results demonstrate that the mitochondria- and possibly also endoplasmic reticulum-dependent pathways are the key apoptotic pathways for heat-induced germ cell death in the testis.


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CRRD Object Information
CRRD ID: 2301325
Created: 2008-10-06
Species: All species
Last Modified: 2008-10-06
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.