A hemodynamic load in vivo induces cardiac expression of the cellular oncogene, c-myc

Sharon L. Mulvagh; Lloyd H. Michael; M. Benjamin Perryman; Robert Roberts; Michael D. Schneider

doi:10.1016/0006-291X(87)90977-6

A hemodynamic load in vivo induces cardiac expression of the cellular oncogene, c-myc

Sharon L. Mulvagh, Lloyd H. Michael, M. Benjamin Perryman, Robert Roberts, Michael D. Schneider

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83 Citas (Scopus)

Resumen

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.

Idioma original	English
Páginas (desde-hasta)	627-636
Número de páginas	10
Publicación	Biochemical and Biophysical Research Communications
Volumen	147
N.º	2
DOI	https://doi.org/10.1016/0006-291X(87)90977-6
Estado	Published - sep. 15 1987
Publicado de forma externa	Sí

Nota bibliográfica

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.

ASJC Scopus Subject Areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

PubMed: MeSH publication types

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

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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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note = "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.",

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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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A hemodynamic load in vivo induces cardiac expression of the cellular oncogene, c-myc

Resumen

Nota bibliográfica

ASJC Scopus Subject Areas

PubMed: MeSH publication types

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