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This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 293/4/H2305    most recent 00361.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wang, B.-W. Articles by Shyu, K.-G. Search for Related Content PubMed PubMed Citation Articles by Wang, B.-W. Articles by Shyu, K.-G.

Mechanical stretch enhances the expression of resistin gene in cultured cardiomyocytes via tumor necrosis factor-

¹Division of Cardiology and ³Department of Emergency Medicine, Shin Kong Wu Ho-Su Memorial Hospital; ²School of Medicine, Fu-Jen Catholic University; and ⁴Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan

Submitted 22 March 2007 ; accepted in final form 7 June 2007

The heart is a resistin target tissue and can function as an autocrine organ. We sought to investigate whether cyclic mechanical stretch could induce resistin expression in cardiomyocytes and to test whether there is a link between the stretch-induced TNF- and resistin. Neonatal Wistar rat cardiomyocytes grown on a flexible membrane base were stretched by vacuum to 20% of maximum elongation at 60 cycles/min. Cyclic stretch significantly increased resistin protein and mRNA expression after 2–18 h of stretch. Addition of PD-98059, TNF- antibody, TNF- receptor antibody, and ERK MAP kinase small interfering RNA 30 min before stretch inhibited the induction of resistin protein. Cyclic stretch increased, whereas PD-98059 abolished, the phosphorylated ERK protein. Gel-shift assay showed a significant increase in DNA-protein binding activity of NF-B after stretch, and PD-98059 abolished the DNA-protein binding activity induced by cyclic stretch. DNA binding complexes induced by cyclic stretch could be supershifted by p65 monoclonal antibody. Cyclic stretch increased resistin promoter activity, whereas PD-98059 and p65 antibody decreased resistin promoter activity. Cyclic stretch significantly increased TNF- secretion from myocytes. Recombinant resistin protein and conditioned medium from stretched cardiomyocytes reduced glucose uptake in cardiomyocytes, and recombinant small interfering RNA of resistin or TNF- antibody reversed glucose uptake. In conclusion, cyclic mechanical stretch enhances resistin expression in cultured rat neonatal cardiomyocytes. The stretch-induced resistin is mediated by TNF-, at least in part, through ERK MAP kinase and NF-B pathways. Glucose uptake in cardiomyocytes was reduced by resistin upregulation.

cyclic stretch; glucose uptake

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