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Adenovirus‐mediated overexpression of cardiac troponin I‐interacting kinase promotes cardiomyocyte hypertrophy
Author(s) -
Wang Lin,
Wang Hui,
Ye Jue,
Xu RuiXia,
Song Li,
Shi Na,
Zhang YanWan,
Chen Xi,
Meng XianMin
Publication year - 2011
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2011.05499.x
Subject(s) - myocyte , western blot , sarcomere , microbiology and biotechnology , muscle hypertrophy , troponin i , protein kinase a , chemistry , kinase , biology , medicine , endocrinology , gene , biochemistry , myocardial infarction
Summary 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 β‐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.