| pubmed-article:20457122 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20457122 | lifeskim:mentions | umls-concept:C0225828 | lld:lifeskim |
| pubmed-article:20457122 | lifeskim:mentions | umls-concept:C1383501 | lld:lifeskim |
| pubmed-article:20457122 | lifeskim:mentions | umls-concept:C0019868 | lld:lifeskim |
| pubmed-article:20457122 | lifeskim:mentions | umls-concept:C2003941 | lld:lifeskim |
| pubmed-article:20457122 | lifeskim:mentions | umls-concept:C0449297 | lld:lifeskim |
| pubmed-article:20457122 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:20457122 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:20457122 | pubmed:dateCreated | 2010-6-14 | lld:pubmed |
| pubmed-article:20457122 | 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. | lld:pubmed |
| pubmed-article:20457122 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20457122 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20457122 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20457122 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20457122 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20457122 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20457122 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20457122 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20457122 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:20457122 | pubmed:issn | 1090-2104 | lld:pubmed |
| pubmed-article:20457122 | pubmed:author | pubmed-author:DannW JWJ | lld:pubmed |
| pubmed-article:20457122 | pubmed:author | pubmed-author:WangYanruY | lld:pubmed |
| pubmed-article:20457122 | pubmed:author | pubmed-author:QuAijuanA | lld:pubmed |
| pubmed-article:20457122 | pubmed:copyrightInfo | (c) 2010 Elsevier Inc. All rights reserved. | lld:pubmed |
| pubmed-article:20457122 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20457122 | pubmed:day | 11 | lld:pubmed |
| pubmed-article:20457122 | pubmed:volume | 396 | lld:pubmed |
| pubmed-article:20457122 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20457122 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20457122 | pubmed:pagination | 894-900 | lld:pubmed |
| pubmed-article:20457122 | pubmed:meshHeading | pubmed-meshheading:20457122... | lld:pubmed |
| pubmed-article:20457122 | pubmed:meshHeading | pubmed-meshheading:20457122... | lld:pubmed |
| pubmed-article:20457122 | pubmed:meshHeading | pubmed-meshheading:20457122... | lld:pubmed |
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| pubmed-article:20457122 | pubmed:meshHeading | pubmed-meshheading:20457122... | lld:pubmed |
| pubmed-article:20457122 | pubmed:meshHeading | pubmed-meshheading:20457122... | lld:pubmed |
| pubmed-article:20457122 | pubmed:meshHeading | pubmed-meshheading:20457122... | lld:pubmed |
| pubmed-article:20457122 | pubmed:meshHeading | pubmed-meshheading:20457122... | lld:pubmed |
| pubmed-article:20457122 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20457122 | pubmed:articleTitle | PGC-1 alpha accelerates cytosolic Ca2+ clearance without disturbing Ca2+ homeostasis in cardiac myocytes. | lld:pubmed |
| pubmed-article:20457122 | pubmed:affiliation | Institute of Molecular Medicine, State Key Laboratory of Biomembrane and Membrane Biotechnology, Peking University, Beijing 100871, China. chenminyx@gmail.com | lld:pubmed |
| pubmed-article:20457122 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20457122 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:83516 | entrezgene:pubmed | pubmed-article:20457122 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:20457122 | lld:entrezgene |
