Source:http://linkedlifedata.com/resource/pubmed/id/20738325
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
11
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| pubmed:dateCreated |
2010-10-27
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| pubmed:abstractText |
1. Our previous study has shown that leptin induces cardiomyocyte hypertrophy; however, the mechanisms are poorly understood. Recent studies have shown that peroxisome proliferator-activated receptor ? (PPAR?) activation might be responsible for pathological remodeling and severe cardiomyopathy. Leptin, as an endogenous activator of PPAR?, regulates energy metabolism through activating PPAR? in many cells. Therefore, we hypothesized that leptin induces cardiomyocyte hypertrophy through activating the cardiac PPAR? pathway. 2. Cultured neonatal rat cardiomyocytes were used to evaluate the effects of PPAR? on hypertrophy. The selective PPAR? antagonist GW6471 concentration-dependently decreased atrial natriuretic factor mRNA expression by 23%, 36%, 44% and 59%, and significantly decreased total RNA levels, protein synthesis and cell surface areas, all of which were elevated by 72h of leptin treatment. The augmentation of reactive oxygen species levels in leptin treated cardiomyocytes was reversed by 0.1-10?mol/L GW6471 (40%, 52% and 58%). After 24h of treatment, leptin concentration-dependently enhanced mRNA expression by 7%, 93%, 100% and 256%, and protein expression by 31.2%, 64.2%, 143% and 199%, and the activity of PPAR?. Meanwhile, cardiomycytes receiving 72h of treatment with the PPAR? agonist, fenofibrate, concentration-dependently increased total RNA levels, atrial natriuretic factor mRNA expression, protein synthesis and cell surface area. Treatment of fenofibrate for 4?h also elevated oxygen species levels in a concentration-dependent manner. 3. In conclusion, these findings show that leptin induces hypertrophy through the activation of the PPAR? pathway in cultured neonatal rat cardiomyocytes.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/GW 6471,
http://linkedlifedata.com/resource/pubmed/chemical/Leptin,
http://linkedlifedata.com/resource/pubmed/chemical/Oxazoles,
http://linkedlifedata.com/resource/pubmed/chemical/PPAR alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species,
http://linkedlifedata.com/resource/pubmed/chemical/Tyrosine
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| pubmed:status |
MEDLINE
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| pubmed:month |
Nov
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| pubmed:issn |
1440-1681
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| pubmed:author | |
| pubmed:copyrightInfo |
© 2010 Blackwell Publishing Asia Pty Ltd.
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| pubmed:issnType |
Electronic
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| pubmed:volume |
37
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1087-95
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| pubmed:meshHeading |
pubmed-meshheading:20738325-Animals,
pubmed-meshheading:20738325-Animals, Newborn,
pubmed-meshheading:20738325-Blotting, Western,
pubmed-meshheading:20738325-Cardiomegaly,
pubmed-meshheading:20738325-Cell Culture Techniques,
pubmed-meshheading:20738325-Cell Enlargement,
pubmed-meshheading:20738325-Cells, Cultured,
pubmed-meshheading:20738325-Dose-Response Relationship, Drug,
pubmed-meshheading:20738325-Electrophoretic Mobility Shift Assay,
pubmed-meshheading:20738325-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:20738325-Leptin,
pubmed-meshheading:20738325-Myocytes, Cardiac,
pubmed-meshheading:20738325-Obesity,
pubmed-meshheading:20738325-Oxazoles,
pubmed-meshheading:20738325-PPAR alpha,
pubmed-meshheading:20738325-Protein Binding,
pubmed-meshheading:20738325-Rats,
pubmed-meshheading:20738325-Reactive Oxygen Species,
pubmed-meshheading:20738325-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:20738325-Tyrosine
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| pubmed:year |
2010
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| pubmed:articleTitle |
Leptin induces hypertrophy through activating the peroxisome proliferator-activated receptor ? pathway in cultured neonatal rat cardiomyocytes.
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| pubmed:affiliation |
Department of Pharmacology, Guangzhou Medical University, China.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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