TY - JOUR
T1 - A hemodynamic load in vivo induces cardiac expression of the cellular oncogene, c-myc
AU - Mulvagh, Sharon L.
AU - Michael, Lloyd H.
AU - Perryman, M. Benjamin
AU - Roberts, Robert
AU - Schneider, Michael D.
N1 - Funding Information:
We thank R.A. Weinberg, C.D. Stiles and R. Schwartz for the plasmids indicated. We are grateful to Gary Liedtke and Peggy Jackson for technical assistance in surgery and to Mark Entman for helpful discussions. This investigation was supported in part by grants from the American Heart Association Texas Affiliate (M.D.S., M.B.P.) and the National Institutes of Health (M.D.S., L.M.). Animal surgery support was provided by the DeBakey Heart Center. The Molecular Cardiology Unit is supported by the American Heart Association Bugher Foundation Center for Molecular Biology of the Cardiovascular System.
PY - 1987/9/15
Y1 - 1987/9/15
N2 - 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.
AB - 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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U2 - 10.1016/0006-291X(87)90977-6
DO - 10.1016/0006-291X(87)90977-6
M3 - Article
C2 - 2958008
AN - SCOPUS:0023473339
SN - 0006-291X
VL - 147
SP - 627
EP - 636
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -