Source:http://linkedlifedata.com/resource/pubmed/id/21314842
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2011-3-25
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pubmed:abstractText |
1. Cardiac troponin I-interacting kinase (TNNI3K) is a novel cardiac-specific kinase gene. Quantitative real-time reverse transcription polymerase chain reaction analysis showed a significant increase in TNNI3K mRNA expression in hypertrophic cardiomyocytes induced by endothelin-1 (ET-1). The aim of the present study was to investigate the effects of TNNI3K on neonate rat cardiomyocyte hypertrophy induced by ET-1. 2. Adenoviruses were amplified in 293A cells. To determine a reasonable adenovirus infection dose cardiomyocytes were infected with an adenovirus carrying human TNNI3K (Ad-TNNI3K) at varying multiplicity of infection (MOI) and the expression of TNNI3K was analysed by western blot. 3. Cardiomyocytes were infected with either a control adenovirus carrying green fluorescent protein (Ad-GFP) or Ad-TNNI3K. Compared with Ad-GFP, the Ad-TNNI3K induced an increase in sarcomere organization, cell surface area, (3) H-leucine incorporation and ?-MHC re-expression. This type of hypertrophic phenomenon is similar to that observed in Ad-GFP-infected hypertrophic cardiomyocytes induced by ET-1. To determine the functional role of TNNI3K in ET-1-induced hypertrophic cardiomyocytes, the cells were infected with Ad-GFP or Ad-TNNI3K. Ad-TNNI3K induced an increase in sarcomere organization, cell surface area and (3) H-leucine incorporation compared with Ad-GFP. 4. These results suggest that TNNI3K overexpression induces cardiomyocytes hypertrophy and accelerates hypertrophy in hypertrophic cardiomyocytes. Therefore, TNNI3K might be an interesting target for the clinical treatment of hypertrophy.
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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/Endothelin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Green Fluorescent Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Leucine,
http://linkedlifedata.com/resource/pubmed/chemical/MAP Kinase Kinase Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/TNNI3K protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Ventricular Myosins
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1440-1681
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pubmed:author | |
pubmed:copyrightInfo |
© 2011 The Authors. Clinical and Experimental Pharmacology and Physiology © 2011 Blackwell Publishing Asia Pty Ltd.
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pubmed:issnType |
Electronic
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pubmed:volume |
38
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
278-84
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pubmed:meshHeading |
pubmed-meshheading:21314842-Adenoviridae,
pubmed-meshheading:21314842-Animals,
pubmed-meshheading:21314842-Cardiomegaly,
pubmed-meshheading:21314842-Cells, Cultured,
pubmed-meshheading:21314842-Endothelin-1,
pubmed-meshheading:21314842-Gene Expression,
pubmed-meshheading:21314842-Green Fluorescent Proteins,
pubmed-meshheading:21314842-Humans,
pubmed-meshheading:21314842-Leucine,
pubmed-meshheading:21314842-MAP Kinase Kinase Kinases,
pubmed-meshheading:21314842-Myocytes, Cardiac,
pubmed-meshheading:21314842-Rats,
pubmed-meshheading:21314842-Rats, Sprague-Dawley,
pubmed-meshheading:21314842-Sarcomeres,
pubmed-meshheading:21314842-Ventricular Myosins
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pubmed:year |
2011
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pubmed:articleTitle |
Adenovirus-mediated overexpression of cardiac troponin I-interacting kinase promotes cardiomyocyte hypertrophy.
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pubmed:affiliation |
Core laboratory, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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