Source:http://linkedlifedata.com/resource/pubmed/id/20457122
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2010-6-14
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pubmed:abstractText |
Energy metabolism and Ca(2+) handling serve critical roles in cardiac physiology and pathophysiology. Peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1 alpha) is a multi-functional coactivator that is involved in the regulation of cardiac mitochondrial functional capacity and cellular energy metabolism. However, the regulation of PGC-1 alpha in cardiac Ca(2+) signaling has not been fully elucidated. To address this issue, we combined confocal line-scan imaging with off-line imaging processing to characterize calcium signaling in cultured adult rat ventricular myocytes expressing PGC-1 alpha via adenoviral transduction. Our data shows that overexpressing PGC-1 alpha improved myocyte contractility without increasing the amplitude of Ca(2+) transients, suggesting that myofilament sensitivity to Ca(2+) increased. Interestingly, the decay kinetics of global Ca(2+) transients and Ca(2+) waves accelerated in PGC-1 alpha-expressing cells, but the decay rate of caffeine-elicited Ca(2+) transients showed no significant change. This suggests that sarcoplasmic reticulum (SR) Ca(2+)-ATPase (SERCA2a), but not Na(+)/Ca(2+) exchange (NCX) contribute to PGC-1 alpha-induced cytosolic Ca(2+) clearance. Furthermore, PGC-1 alpha induced the expression of SERCA2a in cultured cardiac myocytes. Importantly, overexpressing PGC-1 alpha did not disturb cardiac Ca(2+) homeostasis, because SR Ca(2+) load and the propensity for Ca(2+) waves remained unchanged. These data suggest that PGC-1 alpha can ameliorate cardiac Ca(2+) cycling and improve cardiac work output in response to physiological stress. Unraveling the PGC-1 alpha-calcium handling pathway sheds new light on the role of PGC-1 alpha in the therapy of cardiac diseases.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1090-2104
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pubmed:author | |
pubmed:copyrightInfo |
(c) 2010 Elsevier Inc. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:day |
11
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pubmed:volume |
396
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
894-900
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pubmed:meshHeading |
pubmed-meshheading:20457122-Animals,
pubmed-meshheading:20457122-Calcium,
pubmed-meshheading:20457122-Calcium Signaling,
pubmed-meshheading:20457122-Cytosol,
pubmed-meshheading:20457122-Homeostasis,
pubmed-meshheading:20457122-Myocardial Contraction,
pubmed-meshheading:20457122-Myocytes, Cardiac,
pubmed-meshheading:20457122-RNA-Binding Proteins,
pubmed-meshheading:20457122-Rats,
pubmed-meshheading:20457122-Rats, Sprague-Dawley,
pubmed-meshheading:20457122-Stress, Physiological,
pubmed-meshheading:20457122-Transcription Factors
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pubmed:year |
2010
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pubmed:articleTitle |
PGC-1 alpha accelerates cytosolic Ca2+ clearance without disturbing Ca2+ homeostasis in cardiac myocytes.
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pubmed:affiliation |
Institute of Molecular Medicine, State Key Laboratory of Biomembrane and Membrane Biotechnology, Peking University, Beijing 100871, China. chenminyx@gmail.com
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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