BH4-domain peptide from Bcl-xL exerts anti-apoptotic activity in vivo

التفاصيل البيبلوغرافية
العنوان: BH4-domain peptide from Bcl-xL exerts anti-apoptotic activity in vivo
المؤلفون: Toru Kawakami, Hiroshi Tamagawa, Yoshihide Tsujimoto, Rie Sugioka, Toshihiro Funatsu, Yoshiki Sawa, Shigeomi Shimizu
المصدر: Oncogene. 22:8432-8440
بيانات النشر: Springer Science and Business Media LLC, 2003.
سنة النشر: 2003
مصطلحات موضوعية: Cancer Research, bcl-X Protein, Apoptosis, Myocardial Reperfusion Injury, Bcl-xL, Mitochondrion, Biology, Hepatitis, Mice, In vivo, Apoptotic mitochondrial changes, Intestine, Small, Genetics, Animals, Humans, Inner mitochondrial membrane, Molecular Biology, X-Rays, Cytochrome c, Molecular biology, Protein Structure, Tertiary, Cell biology, Proto-Oncogene Proteins c-bcl-2, biology.protein, Peptides, Ex vivo, HeLa Cells
الوصف: The Bcl-2 family of proteins regulates apoptosis chiefly by controlling mitochondrial membrane permeability. It has previously been shown that the BH4 domain of Bcl-2/Bcl-xL is essential for the prevention of apoptotic mitochondrial changes, including the release of cytochrome c and apoptotic cell death. We have previously reported that BH4 peptide fused to the protein transduction domain of HIV-1 TAT protein (TAT-BH4) significantly inhibits etoposide-induced apoptosis in a cell line. This time, we investigated whether TAT-BH4 peptide was cytoprotective in ex vivo and in vivo rodent models. Intraperitoneal injection of TAT-BH4 peptide greatly inhibited X-ray-induced apoptosis in the small intestine of mice and partially suppressed Fas-induced fulminant hepatitis. In addition, this peptide markedly suppressed heart failure after ischemia-reperfusion injury in isolated rat heart, probably by preventing mitochondrial dysfunction. These findings demonstrate that TAT-BH4 peptide exerts anti-apoptotic activity both in vivo and ex vivo, and imply that it may be a useful therapeutic agent for diseases involving mitochondrial dysfunction and apoptosis.
تدمد: 1476-5594
0950-9232
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::47f837fb16f540922ecb25ae3046b410
https://doi.org/10.1038/sj.onc.1207180
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....47f837fb16f540922ecb25ae3046b410
قاعدة البيانات: OpenAIRE