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Cardiovascular Research 1999 42(1):140-148; doi:10.1016/S0008-6363(98)00294-6
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

G{alpha}13 stimulates gene expression and increases cell size in cultured neonatal rat ventricular myocytes

Stephen G. Finna, Steven G. Plonkb and Stephen J. Fullera,*

aCardiac Medicine, NHLI Division, Imperial College School of Medicine, London SW3 6LY, UK
bHoward Hughes Medical Institute, Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, TN 37232, USA

* Corresponding author: Tel.: +44-171-352-8121; ext. 3309/3314; fax: +44-171-823-3392. E-mail address: stephen.fuller@ic.ac.uk

Objectives: Constitutively-active G{alpha}13 causes permissive cell types to proliferate or undergo phenotypic transformation implying a role for G13 in the control of cell growth. Cardiac myocytes are terminally-differentiated cells which respond to growth stimuli by increasing in size rather than by cell division. The objective of this study was to determine whether constitutively-active G{alpha}13 is able to induce a hypertrophic phenotype in cardiac myocytes. Methods: Cultured neonatal rat ventricular myocytes were transiently transfected with an expression vector (pRC/RSV) encoding wild-type G{alpha}13 or constitutively-active G{alpha}13Q226L. Effects on transcription were monitored by co-transfected luciferase (LUX) reporter genes under the control of promoters responsive to hypertrophic stimuli. Cell size was determined by planimetry. Results: Transfection of neonatal myocytes with G{alpha}13Q226L, but not wild-type G{alpha}13, stimulated ANF638LUX and ANF3003LUX expression to 3.0±0.3- and 4.3±0.6-fold of the control, respectively. Likewise, G{alpha}13Q226L stimulated vMLC250LUX and vMLC2700LUX expression to 3.9±1.0- and to 7.7±1.7-fold of controls, respectively, but there was relatively little effect of G{alpha}13Q226L on c-fos-SRE- and β-MHC promoter activity. The effects of G{alpha}13Q226L on ANF3003LUX were inhibited by expression of C3 exoenzyme. Wild-type G{alpha}13 and G{alpha}13Q226L increased myocyte area from 869±43 µm2 in control transfections to 1287±64 µm2 and 1278±59 µm2, respectively. Conclusion: We conclude that G{alpha}13Q226L is able to induce gene expression and morphological changes associated with a hypertrophic response in cardiac myocytes and that the transcriptional effects may be mediated through a Rho-dependent mechanism.

KEYWORDS G-proteins; Myocytes; Rat; Signal transduction; Gene expression; Hypertrophy


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