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

Research output: Contribution to journal › Article › peer-review

83 Citations (Scopus)

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.

Original language	English
Pages (from-to)	627-636
Number of pages	10
Journal	Biochemical and Biophysical Research Communications
Volume	147
Issue number	2
DOIs	https://doi.org/10.1016/0006-291X(87)90977-6
Publication status	Published - Sept 15 1987
Externally published	Yes

Bibliographical 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.

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

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

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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AU - Schneider, Michael D.

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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.

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

Abstract

Bibliographical note

ASJC Scopus Subject Areas

PubMed: MeSH publication types

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