Document Detail


Exercise training decreases store-operated Ca2+entry associated with metabolic syndrome and coronary atherosclerosis.
MedLine Citation:
PMID:  19744946     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
AIMS: Stenting attenuates restenosis, but accelerated coronary artery disease (CAD) adjacent to the stent (peri-stent CAD) remains a concern in metabolic syndrome (MetS). Smooth muscle cell proliferation, a major mechanism of CAD, is mediated partly by myoplasmic Ca2+ dysregulation and store-operated Ca2+ entry (SOCE) via canonical transient receptor potential 1 (TRPC1) channels is proposed to play a key role. Exercise is known to prevent Ca2+ dysregulation in CAD. We tested the hypothesis that MetS increases SOCE and peri-stent CAD and exercise attenuates these events.
METHODS AND RESULTS: Groups (n = 9 pigs each) were (i) healthy lean Ossabaw swine fed standard chow, (ii) excess calorie atherogenic diet fed (MetS), and (iii) aerobically exercise trained starting after 50 weeks of development of MetS (XMetS). Bare metal stents were placed after 54 weeks on diets, and CAD and SOCE were assessed 4 weeks later. Coronary cells were dispersed proximal to the stent (peri-stent) and from non-stent segments, and fura-2 fluorescence was used to assess SOCE, which was verified by Ni2+ blockade and insensitivity to nifedipine. XMetS pigs had increased physical work capacity and decreased LDL/HDL (P < 0.05), but no attenuation of robust insulin resistance, glucose intolerance, hypertriglyceridaemia, or hypertension. CAD was greater in peri-stented vs. non-stented artery segments. MetS had the greatest CAD, SOCE, and TRPC1 and STIM1 mRNA and protein expression, which were all attenuated in XMetS.
CONCLUSION: This is the first report of the protective effect of exercise on native CAD, peri-stent CAD, SOCE, and molecular expression of TRPC1, STIM1, and Orai1 in MetS.
Authors:
Jason M Edwards; Zachary P Neeb; Mouhamad A Alloosh; Xin Long; Ian N Bratz; Cassandra R Peller; James P Byrd; Sanjay Kumar; Alexander G Obukhov; Michael Sturek
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-09-10
Journal Detail:
Title:  Cardiovascular research     Volume:  85     ISSN:  1755-3245     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-01-06     Completed Date:  2010-03-10     Revised Date:  2013-05-31    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  631-40     Citation Subset:  IM    
Affiliation:
Department of Cellular and Integrative Physiology, Indiana University School of Medicine, 635 Barnhill Drive, MS 385, Indianapolis, IN 46202-5120, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Calcium / metabolism*
Coronary Artery Disease / etiology,  metabolism*
Male
Metabolic Syndrome X / complications,  metabolism*
Physical Conditioning, Animal*
Stents
Swine
TRPC Cation Channels / physiology
Grant Support
ID/Acronym/Agency:
HL062552/HL/NHLBI NIH HHS; HL083381/HL/NHLBI NIH HHS; RR013223/RR/NCRR NIH HHS; UL1 RR025761/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/TRPC Cation Channels; 7440-70-2/Calcium
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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