Cardiac myocyte hypertrophy is associated with c-myc protooncogene expression

N. F. Starksen, P. C. Simpson, N. Bishopric, S. R. Coughlin, W. M. Lee, J. A. Escobedo, L. T. Williams

Research output: Contribution to journalArticlepeer-review

215 Scopus citations


The mechanism of hormonally induced cell hypertrophy is unknown. Stimulation of cardiac myocytes by α1-adrenergic agents, phorbol esters, and serum induces an increase in the cell size of nondividing cardiac myocytes in primary culture. Expression of the c-myc gene, known to be increased in growth factor-induced cell division, was studied in this model of cell hypertrophy. The α-adrenergic agonist norepinephrine (0.002-20 μM) increased levels of c-myc-encoded mRNA to 10-fold over control levels. This increase was detectable at 30 min, peaked at 2 hr, and returned to baseline by 6 hr after stimulation. The norepinephrine response was abolished by the α1-antagonist terazosin (2 μM) but was not affected by the β-adrenergic antagonist propranolol (2 μM) and was only slightly (25%) attenuated by the α2-adrenergic antagonist yohimbine (2 μM). Serum and the phorbol ester tumor promoter phorbol 12-myristate 13-acetate also enhanced c-myc expression in cardiac myocyte cultures. These findings show that the induction of cardiac myocyte hypertrophy is associated with enhanced expression of the c-myc gene and suggest that hormonally induced cell hypertrophy and cell division share common mechanistic pathways.

Original languageEnglish (US)
Pages (from-to)8348-8350
Number of pages3
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number21
StatePublished - 1986
Externally publishedYes

ASJC Scopus subject areas

  • General


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