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Role of cytochrom c and Bad protein in post‐ischemic neuronal death – CsA protection
Author(s) -
Dłużniewska J.,
Zabłocka B.,
Kozłowska H.,
Sarnowska A.,
DomańskaJanik K.
Publication year - 2003
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.85.s2.18_3.x
Subject(s) - ischemia , mitochondrion , cytosol , apoptosis , cytochrome c , mitochondrial permeability transition pore , microbiology and biotechnology , pharmacology , chemistry , in vitro , chromosomal translocation , programmed cell death , biology , medicine , biochemistry , enzyme , gene
We have estimated cytosolic cytochrom c (cCyt c) as a measure of mitochondria permeability (MP) and its inhibition by CsA. In hippocampus of gerbils subjected to 5 min ischemia, cCyt c increased biphasically: transiently at 0.5 h and then steadily at ≥24 h. Involvement of proapoptotic protein Bad in the mechanism of MP after ischemia was studied too. Immediate interarterial infusion of CsA (10 mg/kg) totally inhibited early Cyt c translocation and protected CA1 neurons. This effect disappears with delayed application of the drug. Temporal ability of CsA to block apoptotic signaling and Cyt c translocation was verified on primary cortical neurons in vitro by confocal immuno‐imaging. The results confirm time‐limited effectiveness of CsA to inhibit mitochondrial cyclophilin D connected permeability to Cyt c and to protect hippocampus by relatively narrow ‘window of opportunity’ after ischemic insult. Acknowledgements: Supported by PBZ‐KBN‐002/CD/P05/2000 and statutory theme 4.