| Acute exercise activates myocardial nuclear factor kappa B. | |
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MedLine Citation:
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PMID: 20694538 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The myocardial stress response to exercise is dependent on exercise intensity and thus understanding the molecular responses between various exercise intensity levels might aid in exercise prescription. Nuclear factor kappa B (NF-κB) is a ubiquitous transcription factor that mediates a variety of cellular processes including inflammation, immune responses, apoptosis and cell growth/development. NF-κB can be comprised of homo- and/or heterodimers formed from five distinct proteins: p50 (NF-κB1), p52 (NF-κB2), RelA (p65), c-Rel, and RelB. NF-κB is located in the cytoplasm and kept inactive by inhibitory proteins but following the exposure to a myriad of stimuli, an activated NF-κB dimer translocates to the nucleus and exerts transcriptional effects on upwards of 150 genes. To examine the activation of NF-κB in the myocardium following exercise, male Sprague-Dawley rats (n = 24) were exercised by treadmill running at 20 m/min for 30 min or 30 m/min for 20 min. At 0, 2, or 24 h following exercise, animals were anesthetized, hearts excised and immediately frozen in liquid nitrogen. Portions of hearts were homogenized, protein concentrations determined and extracts assayed for NF-κB activation (DNA binding activity) using electrophoretic mobility shift assays (EMSA). Visual examination of EMSA autoradiographs revealed an enhanced NF-κB activation in the hearts from exercised animals when compared with non-running controls. Subsequent supershift analyses using antibodies specific for NF-κB subunits showed the higher intensity exercise was associated with p65 (RelA) in the activated NF-κB complex while the NF-κB complex in hearts from animals exercised at the lower intensity was comprised primarily of p50. These data suggest exercise is capable of activating myocardial NF-κB and that a threshold for the activation of specific NF-κB subunits may exist. |
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Authors:
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Marko Balan; Marius Locke |
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Publication Detail:
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Type: Journal Article Date: 2010-08-06 |
Journal Detail:
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Title: Cell stress & chaperones Volume: 16 ISSN: 1466-1268 ISO Abbreviation: Cell Stress Chaperones Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2010-12-02 Completed Date: 2011-03-16 Revised Date: 2011-08-01 |
Medline Journal Info:
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Nlm Unique ID: 9610925 Medline TA: Cell Stress Chaperones Country: Netherlands |
Other Details:
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Languages: eng Pagination: 105-11 Citation Subset: IM |
Affiliation:
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Faculty of Physical Education and Health, University of Toronto, 55 Harbord Street, Toronto, ON, M5S 2W6, Canada. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Dimerization Electrophoretic Mobility Shift Assay Male Myocardium / metabolism* NF-kappa B / metabolism* NF-kappa B p50 Subunit / metabolism NF-kappa B p52 Subunit / metabolism Physical Conditioning, Animal Rats Rats, Sprague-Dawley Temperature Time Factors Transcription Factor AP-1 / metabolism Transcription Factor RelA / metabolism Transcription Factor RelB / metabolism |
| Chemical | |
Reg. No./Substance:
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0/NF-kappa B; 0/NF-kappa B p50 Subunit; 0/NF-kappa B p52 Subunit; 0/Transcription Factor AP-1; 0/Transcription Factor RelA; 147337-75-5/Transcription Factor RelB |
| Comments/Corrections | |
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