| Ischemia reperfusion injury, KATP channels, and exercise-induced cardioprotection against apoptosis. | |
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MedLine Citation:
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PMID: 22653992 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Exercise is a potent stimulus against cardiac ischemia reperfusion (IR) injury, although the protective mechanisms are not completely understood. The study purpose was to examine whether the mitochondrial or sarcolemmal ATP-sensitive potassium channel (mito K(ATP) or sarc K(ATP), respectively) mediates exercise-induced cardioprotection against post-IR cell death and apoptosis. Eighty-six, 4-mo-old male Sprague Dawley rats were randomly assigned to treadmill exercise (Ex; 30 m/min, 3 days, 60 min, ∼70 maximal oxygen uptake) and sedentary (Sed) treatments. Rats were exposed to regional cardiac ischemia (50 min) and reperfusion (120 min) or Sham (170 min; no ligation) surgeries. Exercise subgroups received placebo (saline), 5-hydroxydecanoate (5HD; 10 mg/kg ip), or HMR1098 (10 mg/kg ip) to inhibit mito K(ATP) or sarc K(ATP) channel. Comprehensive outcome assessments included post-IR ECG arrhythmias, cardiac tissue necrosis, redox perturbations, and autophagy biomarkers. No arrhythmia differences existed between exercised and sedentary hearts following extended-duration IR (P < 0.05). The sarc K(ATP) channel was confirmed essential (P = 0.002) for prevention of antinecrotic tissue death with exercise (percent infarct, Sed = 42%; Ex = 20%; Ex5HD = 16%; ExHMR = 42%), although neither the mito K(ATP) (P = 0.177) nor sarc K(ATP) (P = 0.274) channel provided post-IR protection against apoptosis (terminal deoxynucleotidyl transferase deoxy UTP-mediated nick-end labeling-positive nuclei/mm(2), Sham = 1.8 ± 0.5; Sed = 19.4 ± 6.7; Ex = 7.5 ± 4.6; Ex5HD = 14.0 ± 3.9; ExHMR = 11.1 ± 1.8). Exercise preconditioning also appears to preserve basal autophagy levels, as assessed by Beclin 1 (P ≤ 0.001), microtubule-associated protein-1 light-chain 3B ratios (P = 0.020), and P62 (P ≤ 0.001), in the hours immediately following IR. Further research is needed to better understand these findings and corresponding redox changes in exercised hearts. |
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Authors:
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John C Quindry; Lindsey Miller; Graham McGinnis; Brian Kliszczewicz; J Megan Irwin; Michael Landram; Zea Urbiztondo; Gayani Nanayakkara; Rajesh Amin |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2012-05-31 |
Journal Detail:
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Title: Journal of applied physiology (Bethesda, Md. : 1985) Volume: 113 ISSN: 1522-1601 ISO Abbreviation: J. Appl. Physiol. Publication Date: 2012 Aug |
Date Detail:
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Created Date: 2012-08-02 Completed Date: 2013-01-08 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 8502536 Medline TA: J Appl Physiol Country: United States |
Other Details:
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Languages: eng Pagination: 498-506 Citation Subset: IM |
Affiliation:
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Cardioprotection Laboratory, Department of Kinesiology, Auburn University, Auburn, Alabama 36830, USA. jcq0001@auburn.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Anti-Arrhythmia Agents / pharmacology Apoptosis / drug effects, physiology* Apoptosis Regulatory Proteins / analysis Autophagy / physiology Decanoic Acids / pharmacology Electrocardiography Glucuronides / pharmacology Hydroxy Acids / pharmacology KATP Channels / antagonists & inhibitors, physiology* Male Microtubule-Associated Proteins / analysis Mitochondria, Heart / drug effects, physiology Myocardial Reperfusion Injury / drug therapy, physiopathology, prevention & control* Oxygen Consumption / drug effects, physiology Physical Conditioning, Animal / physiology* Rats Rats, Sprague-Dawley Sarcolemma / drug effects, physiology Sulfonamides / pharmacology Transcription Factors / analysis |
| Grant Support | |
ID/Acronym/Agency:
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HL087256/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Anti-Arrhythmia Agents; 0/Apoptosis Regulatory Proteins; 0/Decanoic Acids; 0/Glucuronides; 0/Gtf2h1 protein, mouse; 0/HMR 1098 glucuronide; 0/Hydroxy Acids; 0/KATP Channels; 0/MAP1LC3 protein, mouse; 0/Microtubule-Associated Proteins; 0/Sulfonamides; 0/Transcription Factors; 0/beclin 1 protein, rat; 624-00-0/5-hydroxydecanoic acid |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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