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European Heart Journal 1995 16(Supplement C):8-11; doi:10.1093/eurheartj/16.suppl_C.8
Copyright © 1995 by the European Society of Cardiology.
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© 1995 The European Society of Cardiology

Protein kinase cascade activated by mechanical stress in cardiocytes: possible involvement of angiotensin II

I. Kumuro*, T. Yamazaki, Y. Katoh, I. Shiojima, K. Tobe, T. Kadowaki, R. Nagai and Y. Yazaki

Department of Medicine III, Univeristy of Tokyo Japan

Correspondence: I. Komuro, Department of Medicine III, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan

Mechanical stress induces cardiac hypertrophy and expression of specific genes in the cardiac myocytes. External stimuli are generally transduced into the nucleus through the activation of a protein kinase cascade. We have previously shown that stretching cardiomyocyles stimulates the activity of protein kinase C (PKC), mitogen-activated protein (MAP) kinase and S6 protein kinase. In the present study, we examined two other kinases, Raf-1 kinase and MAP kinase kinase, which are supposed to lie between PKC and MAP kinase in the protein kinase cascade. Stretching cardiocytes by using the in vitro system induced hyperphosphorylation of Raf-1 kinase and activation of MAP kinase kinase. The protein kinases activated by mechanical stress are similar to those activated by growth factors. We examined the possible involvement of angiotensin II (Ang II) in the protein synthesis and gene expression induced by mechanical stress. CV11974, an Ang ll-receptor antagonist, partially suppressed the increases in amino acid incorporation, c-fos gene expression and MAP kinase activity induced by stretching. These results suggest that a variety of protein kinases are activated by mechanical stress and that locally produced Angll may in part play important roles in converting mechanical stimuli into biochemical signals

Key Words: Mechanical stress • cardiac hypertrophy • gene expression • protein kinase • angiotensis II


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