Advertisement

Research Article Free access | 10.1172/JCI2552

A requirement for the rac1 GTPase in the signal transduction pathway leading to cardiac myocyte hypertrophy.

J B Pracyk, K Tanaka, D D Hegland, K S Kim, R Sethi, I I Rovira, D R Blazina, L Lee, J T Bruder, I Kovesdi, P J Goldshmidt-Clermont, K Irani, and T Finkel

Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Pracyk, J. in: PubMed | Google Scholar

Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Tanaka, K. in: PubMed | Google Scholar

Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Hegland, D. in: PubMed | Google Scholar

Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Kim, K. in: PubMed | Google Scholar

Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Sethi, R. in: PubMed | Google Scholar

Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Rovira, I. in: PubMed | Google Scholar

Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Blazina, D. in: PubMed | Google Scholar

Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Lee, L. in: PubMed | Google Scholar

Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Bruder, J. in: PubMed | Google Scholar

Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Kovesdi, I. in: PubMed | Google Scholar

Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Goldshmidt-Clermont, P. in: PubMed | Google Scholar

Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Irani, K. in: PubMed | Google Scholar

Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Finkel, T. in: PubMed | Google Scholar

Published September 1, 1998 - More info

Published in Volume 102, Issue 5 on September 1, 1998
J Clin Invest. 1998;102(5):929–937. https://doi.org/10.1172/JCI2552.
© 1998 The American Society for Clinical Investigation
Published September 1, 1998 - Version history
View PDF
Abstract

We have used adenoviral-mediated gene transfer of a constitutively active (V12rac1) and dominant negative (N17rac1) isoform of rac1 to assess the role of this small GTPase in cardiac myocyte hypertrophy. Expression of V12rac1 in neonatal cardiac myocytes results in sarcomeric reorganization and an increase in cell size that is indistinguishable from ligand-stimulated hypertrophy. In addition, V12rac1 expression leads to an increase in atrial natriuretic peptide secretion. In contrast, expression of N17rac1, but not a truncated form of Raf-1, attenuated the morphological hypertrophy associated with phenylephrine stimulation. Consistent with the observed effects on morphology, expression of V12rac1 resulted in an increase in new protein synthesis, while N17rac1 expression inhibited phenylephrine-induced leucine incorporation. These results suggest rac1 is an essential element of the signaling pathway leading to cardiac myocyte hypertrophy.

Version history
  • Version 1 (September 1, 1998): No description
Advertisement
Advertisement