2024-03-28T15:31:02Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/894222017-07-21T12:55:46Zcom_10261_105com_10261_1col_10261_358
Neutral sphingomyelinase-induced ceramide triggers germinal vesicle breakdown and oxidant-dependent apoptosis in Xenopus laevis oocytes
Coll, Olga
Morales, Albert
Fernández-Checa, José C.
García-Ruiz, Carmen
Mitochondria
Reactive oxygen species
Cell death
Reduced glutathione
Ceramide regulates many cellular processes, including cell growth, differentiation, and apoptosis. Although the effects of exogenous bacterial neutral sphingomyelinase (SMase) in Xenopus laevis oocytes have been investigated, its microinjection into oocytes has not been reported previously. Thus, we compared the incubation versus microinjection of the neutral Bacillus cereus sphingomyelinase (bSMase) to examine whether the topology of ceramide generation determines its effects on the fate of oocytes. In agreement with previous findings, incubation of mature stage VI oocytes with bSMase increased ceramide levels in oocyte extracts over time, causing the germinal vesicle breakdown indicative of maturation, without evidence of cytotoxicity. In contrast, bSMase microinjection, which increased ceramide levels in a time- and dose-dependent manner, resulted in oocyte apoptosis characterized by reactive oxygen species (ROS) generation, reduced glutathione (GSH) depletion in cytosol and mitochondria, release of cytochrome c and Smac/Diablo from mitochondria, and caspase-3 activation. Microinjection of acidic SMase from human placenta recapitulated the apoptotic effects of bSMase microinjection. Preincubation of oocytes with GSH-ethyl ester before bSMase microinjection prevented ROS generation and mitochondrial downstream events, thus protecting oocytes from bSMase-induced death. These findings show a divergent action of bSMase-induced ceramide on oocyte maturation or apoptosis depending on the intracellular site where ceramide is generated.
2014-01-14T13:46:27Z
2014-01-14T13:46:27Z
2007-09
artículo
Journal of Lipid Research 48(9): 1924-1935 (2007)
0022-2275
http://hdl.handle.net/10261/89422
10.1194/jlr.M700069-JLR200
1539-7262
eng
http://dx.doi.org/10.1194/jlr.M700069-JLR200
closedAccess
American Society for Biochemistry and Molecular Biology