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Possible participation of mitochondrial lipid rafts in reperfusion‐induced apoptosis
Author(s) -
Martinez Eduardo,
Zazueta Cecilia
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.261
Subject(s) - voltage dependent anion channel , mitochondrial permeability transition pore , mitochondrion , cytochrome c , apoptosis , mptp , mitochondrial apoptosis induced channel , chemistry , adenine nucleotide translocator , ceramide , microbiology and biotechnology , western blot , biology , biochemistry , programmed cell death , bacterial outer membrane , endocrinology , dopaminergic , escherichia coli , dopamine , gene
TNF‐induced apoptosis has been associated to the presence of mitochondrial lipid rafts (MLR) in T‐cells. Recently, we determined that in ischemic‐reperfused hearts (I/R), cytochrome c is released from mitochondria after mitochondrial permeability transition pore (mPTP) opening and Bax insertion into the mitochondria. Also we have reported that cholesterol is relevant for Bax interaction with the mPTP in isolated mitochondria. Thus, the purpose of this work was to investigate a possible role of MLR in reperfusion apoptotic signaling. Mitochondria isolated from I/R rat hearts were treated with 1% TX100 to obtain the MLR insoluble fractions. mPTP‐ forming proteins and lipids in MLR were analyzed by western blot and thin layer chromatography, respectively. The voltage‐dependent anion channel (VDAC) was preferentially partitioned into MLR. The adenine nucleotide translocator (ANT) was found in the TX100 soluble and insoluble fractions. MLR from I/R hearts were enriched with Bax and ceramide, in comparison to non‐ischemic hearts. Our results showed that I/R induced Bax translocation to the mitochondria into TX100‐resistant domains, which are enriched with ceramide and VDAC. Therefore we suggest that MLR could be preferential sites for Bax interaction with the mPTP in I/R‐induced apoptosis. Partial support by grant 46456 to CZ from CONACyT (Consejo Nacional de Ciencia y Tecnología), México .