| Angiotensin preconditioning of the heart: evidence for redox signaling. | |
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MedLine Citation:
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PMID: 16456238 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Angiotensin II (Ang II) has been found to exert preconditioning-like effect on mammalian hearts. Diverse mechanisms are known to exist to explain the cardioprotective abilities of Ang II preconditioning. The present study hypothesized, based on the recent report that Ang II generates reactive oxygen species (ROS) through NADPH oxidase, that Ang II preconditioning occurs through redox cycling. To test this hypothesis, a group of rat hearts was treated with Ang II in the absence or presence of an NADPH oxidase inhibitor, apocynin; or a cell-permeable ROS scavenger, N-acetyl cysteine (NAC). Ang II pretreatment improved postischemic ventricular recovery; reduced myocardial infarction; and decreased the number of cardiomyocyte apoptosis, indicating its ability to precondition the heart against ischemic injury. Both apocynin and NAC almost abolished the preconditioning ability of Ang II. Ang II resulted in increase in ROS activity in the heart, which was reduced by either NAC or apocynin. Ang II also increased both the NADPH oxidase subunits gp91 phox and p22phox mRNA expression, which was abolished with apocynin and NAC. Our results thus demonstrate that the Ang II preconditioning was associated with enhanced ROS activities and increased NADPH oxidase subunits p22phox and gp91phox expression. Both NAC and apocynin reduced ROS activities simultaneously abolishing preconditioning ability of Ang II, suggesting that Ang II preconditioning occurs through redox cycling. That both NAC and apocynin reduced ROS activities and abolished Ang II-mediated increase in p22phox and gp91phox activity further suggest that such redox cycling occurs via both NADPH oxidase-dependent and -independent pathways. |
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Authors:
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Samarjit Das; Richard M Engelman; Nilanjana Maulik; Dipak K Das |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: Cell biochemistry and biophysics Volume: 44 ISSN: 1085-9195 ISO Abbreviation: Cell Biochem. Biophys. Publication Date: 2006 |
Date Detail:
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Created Date: 2006-02-03 Completed Date: 2006-04-05 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 9701934 Medline TA: Cell Biochem Biophys Country: United States |
Other Details:
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Languages: eng Pagination: 103-10 Citation Subset: IM |
Affiliation:
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Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, CT, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acetophenones
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pharmacology Acetylcysteine / pharmacology Angiotensin II / pharmacology* Animals Antioxidants / pharmacology Apoptosis / drug effects Gene Expression / drug effects Heart / drug effects Heart Rate / drug effects Ischemic Preconditioning, Myocardial* Male Membrane Glycoproteins / genetics Membrane Transport Proteins / genetics Myocardial Infarction / etiology, metabolism, pathology Myocardial Reperfusion Injury / complications Myocardium / metabolism Myocytes, Cardiac / drug effects, metabolism NADPH Oxidase / genetics Oxidation-Reduction Perfusion Phosphoproteins / genetics RNA, Messenger / genetics, metabolism Rats Rats, Sprague-Dawley Reactive Oxygen Species / metabolism Reverse Transcriptase Polymerase Chain Reaction Signal Transduction / drug effects*, physiology Ventricular Function, Left / drug effects Ventricular Remodeling / drug effects |
| Grant Support | |
ID/Acronym/Agency:
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HL 22559/HL/NHLBI NIH HHS; HL 33889/HL/NHLBI NIH HHS; HL 34360/HL/NHLBI NIH HHS; HL 56803/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Acetophenones; 0/Antioxidants; 0/Membrane Glycoproteins; 0/Membrane Transport Proteins; 0/Phosphoproteins; 0/RNA, Messenger; 0/Reactive Oxygen Species; 11128-99-7/Angiotensin II; 498-02-2/acetovanillone; 616-91-1/Acetylcysteine; EC 1.6.-/Cybb protein, rat; EC 1.6.3.1/CYBA protein, human; EC 1.6.3.1/NADPH Oxidase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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