A hemodynamic load in vivo induces cardiac expression of the cellular oncogene, c-myc |
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| Authors: | S L Mulvagh L H Michael M B Perryman R Roberts M D Schneider |
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| Affiliation: | 1. Department of Neuroscience, University of Minnesota, Minneapolis, MN, USA;2. Center for NeuroGenetics, Department of Molecular Genetics & Microbiology and Neurology, College of Medicine, Genetics Institute, University of Florida, Gainesville, FL, USA;1. College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, Heilongjiang 150086, China;2. Department of Clinical Pharmacy, The Second Affiliated Hospital, Department of Pharmacology, College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150086, China |
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| Abstract: | To establish whether a hemodynamic load that causes cardiac hypertrophy in the intact animal might interact with cellular pathways that are thought to transduce growth signals in model systems, we have analyzed expression of the cellular oncogene, c-myc, after a systolic pressure load. Aortic constriction increased c-myc mRNA abundance in both the atria and left ventricle of 28-day rats, but did not activate a second "competence" gene, r-fos, whose expression by cardiac cells ceases upon termination of mitotic growth. In 80-day rats, c-myc was induced in the atria alone. Induction of c-myc by aortic constriction in vivo may correlate with the respective capacity of atrial and ventricular myocytes to replicate DNA during cardiac hypertrophy. Activation of c-myc was not sufficient to account for inhibition of muscle creatine kinase (mck) mRNA, which was decreased only in 28-day rats. |
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