G alpha 13 stimulates gene expression and increases cell size in cultured neonatal rat ventricular myocytes.
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 beta-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 micron 2 in control tranfections to 1287 +/- 64 micron 2 and 1278 +/- 59 microns, 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.[1]References
- G alpha 13 stimulates gene expression and increases cell size in cultured neonatal rat ventricular myocytes. Finn, S.G., Plonk, S.G., Fuller, S.J. Cardiovasc. Res. (1999) [Pubmed]
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