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Induction of apoptosis mediated by Fas receptor and activation of caspase-3 in MRL-+/+ or MRL-lpr/lpr murine oocytes

Published online by Cambridge University Press:  09 April 2002

Maowu Guo ,
Eimei Sato ,
Xiang Li ,
Etsuko Mori ,
Shigeru Saito  and
Tsuneatsu Mori
Maowu Guo
Affiliation:
Department of Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-0071, Japan
Eimei Sato
Affiliation:
Laboratory of Animal Reproduction, Graduate School of Agriculture Science, Tohoku University, Sendai 981-8555, Japan
Xiang Li
Affiliation:
Laboratory of Animal Reproduction, Graduate School of Agriculture Science, Tohoku University, Sendai 981-8555, Japan
Etsuko Mori
Affiliation:
Department of Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108-0071, Japan
Shigeru Saito
Affiliation:
Department of Obstetrics and Gynecology, Toyama Medical & Pharmaceutical University, Toyama 930-0194, Japan
Tsuneatsu Mori
Affiliation:
Department of Obstetrics and Gynecology, Toyama Medical & Pharmaceutical University, Toyama 930-0194, Japan
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Abstract

The molecular mechanisms leading to ovarian follicular atresia in the typical pathways of programmed cell death remain to be clarified. Here we have demonstrated that the apoptotic signalling pathway in MRL-+/+ (MRL/+) murine oocytes is through the Fas receptor followed by the activation of caspase-3. In contrast, we found that the aberrant expression and dysfunction of the mutant Fas receptor in MRL-lpr/lpr (MRL/lpr) murine oocytes caused by insertion of the early transposable element (ETn) into the Fas gene were associated with an inability to activate the caspase cascade (especially caspase-3) and to induce nuclear DNA fragmentation. These findings indicate that the induction of apoptosis in MRL/lpr murine oocytes did not occur in the presence of a defective Fas receptor lacking the death domain to trigger the caspase cascade, suggesting a failure to induce ovarian follicular atresia.

Keywords

ApoptosisAtresiaCaspase-3FasOocyte
Type
Research Article
Information
Zygote , Volume 10 , Issue 1 , February 2002 , pp. 17 - 22
Copyright
2002 Cambridge University Press

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