| The late phase of ischemic preconditioning induces a prosurvival genetic program that results in marked attenuation of apoptosis. | |
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MedLine Citation:
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PMID: 17490677 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Although the cardioprotection afforded by the late phase of ischemic preconditioning (PC) in ischemia/reperfusion (I/R) injury has been well studied, it is unknown whether this beneficial effect can be attributed to inhibition of apoptosis. We hypothesized that ischemic PC affords protection by suppressing apoptosis and examined the underlying mechanisms. Myocardial infarction was produced in mice (30-min coronary occlusion). In animals preconditioned 24 h earlier with six 4-min coronary occlusion/4-min reperfusion (O/R) cycles, there was a marked decrease in apoptosis as assessed by three different parameters: hairpin-1 assay, caspase-3 activity, and immunohistochemical analysis of active caspase-3 and cleaved poly (ADP-ribose) polymerase-1 (PARP-1). This protective effect was accompanied by increased expression of multiple antiapoptotic proteins that regulate both the mitochondria-mediated (Bcl-x(L) and Mcl-1) and the death-receptor-mediated (c-FLIP(L) and c-FLIP(S)) pathway of apoptosis and by decreased expression of the proapoptotic protein Bad. This is the first demonstration that the late phase of ischemic PC attenuates cardiac apoptosis after ischemia/reperfusion injury and that this salubrious effect is associated with a complex genetic prosurvival program that results in modulation of several key proteins involved in both the mitochondrial and the death receptor pathways of apoptosis. |
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Authors:
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Adam B Stein; Roberto Bolli; Yiru Guo; Ou-Li Wang; Wei Tan; Wen-Jian Wu; Xiaoping Zhu; Yanqing Zhu; Yu-Ting Xuan |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2007-04-04 |
Journal Detail:
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Title: Journal of molecular and cellular cardiology Volume: 42 ISSN: 0022-2828 ISO Abbreviation: J. Mol. Cell. Cardiol. Publication Date: 2007 Jun |
Date Detail:
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Created Date: 2007-06-04 Completed Date: 2007-08-15 Revised Date: 2011-09-26 |
Medline Journal Info:
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Nlm Unique ID: 0262322 Medline TA: J Mol Cell Cardiol Country: England |
Other Details:
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Languages: eng Pagination: 1075-85 Citation Subset: IM |
Affiliation:
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Department of Medicine and the Institute of Molecular Cardiology, University of Louisville, 570 S. Preston Street, Louisville, KY 40202-1757, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / physiology* CASP8 and FADD-Like Apoptosis Regulating Protein / genetics, metabolism Caspase 3 / analysis, metabolism* Enzyme Activation Immunohistochemistry Ischemic Preconditioning* Male Mice Mice, Inbred ICR Neoplasm Proteins / genetics, metabolism Poly(ADP-ribose) Polymerases / metabolism* Proto-Oncogene Proteins c-bcl-2 / genetics, metabolism Time Factors bcl-2-Associated X Protein / genetics, metabolism bcl-Associated Death Protein / genetics, metabolism bcl-X Protein / genetics, metabolism |
| Grant Support | |
ID/Acronym/Agency:
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HL 55757/HL/NHLBI NIH HHS; HL 68088/HL/NHLBI NIH HHS; HL 70897/HL/NHLBI NIH HHS; HL 76794/HL/NHLBI NIH HHS; P01 HL 78825/HL/NHLBI NIH HHS; P01 HL078825-030003/HL/NHLBI NIH HHS; R01 HL 65660/HL/NHLBI NIH HHS; R01 HL065660-05A2/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Bad protein, mouse; 0/Bax protein, mouse; 0/Bcl2l1 protein, mouse; 0/CASP8 and FADD-Like Apoptosis Regulating Protein; 0/Cflar protein, mouse; 0/Neoplasm Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/bcl-2-Associated X Protein; 0/bcl-Associated Death Protein; 0/bcl-X Protein; 0/myeloid cell leukemia sequence 1 protein; EC 2.4.2.30/Parp1 protein, mouse; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; EC 3.4.22.-/Caspase 3 |
| Comments/Corrections | |
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