Changes in β-actin mRNA expression in remodeling canine myocardium

Wenda C. Carlyle, Cynthia A. Toher, Jonathan R. Vandervelde, Kenneth M. McDonald, David C. Homans, Jay N. Cohn

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Beta-actin, a cytoskeletal protein important in the maintenance of cytoarchitecture, has long been thought to be expressed constitutively in myocardial tissue. As such, β-actin mRNA has been used as a control gene in a wide range of experiments. However, we have uncovered consistent changes in β-actin mRNA expression in canine myocardium remodeling as a result of insult to the left ventricle. The experimental canine models used were either DC shock damage to the left ventricle or volume overload resulting from severe mitral regurgitation. The remodeling process in both canine models is characterized by an increase in left ventricular mass. PCR amplification using primers designed to selectively amplify the 3' end and a portion of the 3' untranslated region of β-actin mRNA resulted in the generation of a 297 base pair product predominant only in normal canine myocardium and a 472 base pair product that became increasingly prominent from 1 to 30 days after DC shock damage to the left ventricle and from 10 to 90 days after creation of mitral regurgitation. Northern analysis showed a three-fold increase in β-actin mRNA after either DC shock or creation of mitral regurgitation. Western analysis revealed an early increase in β-actin protein followed by an apparent decrease to below baseline levels. These observations suggest that changes in β-actin mRNA expression accompany the structural alterations that occur in response to myocardial damage. Whether or not the changes in β-actin mRNA expression play a role in mediating these structural alterations remains to be determined.

Original languageEnglish (US)
Pages (from-to)53-63
Number of pages11
JournalJournal of Molecular and Cellular Cardiology
Volume28
Issue number1
DOIs
StatePublished - Jan 8 1996

Fingerprint

Canidae
Actins
Myocardium
Messenger RNA
Mitral Valve Insufficiency
Heart Ventricles
Shock
Base Pairing
Cytoskeletal Proteins
3' Untranslated Regions
Theoretical Models
Maintenance
Polymerase Chain Reaction
Genes
Proteins

Keywords

  • Canine gene expression
  • Cytoskeletal protein
  • DC shock
  • Mitral regurgitation
  • Ventricular remodeling
  • β-actin

Cite this

Changes in β-actin mRNA expression in remodeling canine myocardium. / Carlyle, Wenda C.; Toher, Cynthia A.; Vandervelde, Jonathan R.; McDonald, Kenneth M.; Homans, David C.; Cohn, Jay N.

In: Journal of Molecular and Cellular Cardiology, Vol. 28, No. 1, 08.01.1996, p. 53-63.

Research output: Contribution to journalArticle

Carlyle, Wenda C. ; Toher, Cynthia A. ; Vandervelde, Jonathan R. ; McDonald, Kenneth M. ; Homans, David C. ; Cohn, Jay N. / Changes in β-actin mRNA expression in remodeling canine myocardium. In: Journal of Molecular and Cellular Cardiology. 1996 ; Vol. 28, No. 1. pp. 53-63.
@article{69259e4929674b2485f098cd97ccb635,
title = "Changes in β-actin mRNA expression in remodeling canine myocardium",
abstract = "Beta-actin, a cytoskeletal protein important in the maintenance of cytoarchitecture, has long been thought to be expressed constitutively in myocardial tissue. As such, β-actin mRNA has been used as a control gene in a wide range of experiments. However, we have uncovered consistent changes in β-actin mRNA expression in canine myocardium remodeling as a result of insult to the left ventricle. The experimental canine models used were either DC shock damage to the left ventricle or volume overload resulting from severe mitral regurgitation. The remodeling process in both canine models is characterized by an increase in left ventricular mass. PCR amplification using primers designed to selectively amplify the 3' end and a portion of the 3' untranslated region of β-actin mRNA resulted in the generation of a 297 base pair product predominant only in normal canine myocardium and a 472 base pair product that became increasingly prominent from 1 to 30 days after DC shock damage to the left ventricle and from 10 to 90 days after creation of mitral regurgitation. Northern analysis showed a three-fold increase in β-actin mRNA after either DC shock or creation of mitral regurgitation. Western analysis revealed an early increase in β-actin protein followed by an apparent decrease to below baseline levels. These observations suggest that changes in β-actin mRNA expression accompany the structural alterations that occur in response to myocardial damage. Whether or not the changes in β-actin mRNA expression play a role in mediating these structural alterations remains to be determined.",
keywords = "Canine gene expression, Cytoskeletal protein, DC shock, Mitral regurgitation, Ventricular remodeling, β-actin",
author = "Carlyle, {Wenda C.} and Toher, {Cynthia A.} and Vandervelde, {Jonathan R.} and McDonald, {Kenneth M.} and Homans, {David C.} and Cohn, {Jay N.}",
year = "1996",
month = "1",
day = "8",
doi = "10.1006/jmcc.1996.0006",
language = "English (US)",
volume = "28",
pages = "53--63",
journal = "Journal of Molecular and Cellular Cardiology",
issn = "0022-2828",
publisher = "Academic Press Inc.",
number = "1",

}

TY - JOUR

T1 - Changes in β-actin mRNA expression in remodeling canine myocardium

AU - Carlyle, Wenda C.

AU - Toher, Cynthia A.

AU - Vandervelde, Jonathan R.

AU - McDonald, Kenneth M.

AU - Homans, David C.

AU - Cohn, Jay N.

PY - 1996/1/8

Y1 - 1996/1/8

N2 - Beta-actin, a cytoskeletal protein important in the maintenance of cytoarchitecture, has long been thought to be expressed constitutively in myocardial tissue. As such, β-actin mRNA has been used as a control gene in a wide range of experiments. However, we have uncovered consistent changes in β-actin mRNA expression in canine myocardium remodeling as a result of insult to the left ventricle. The experimental canine models used were either DC shock damage to the left ventricle or volume overload resulting from severe mitral regurgitation. The remodeling process in both canine models is characterized by an increase in left ventricular mass. PCR amplification using primers designed to selectively amplify the 3' end and a portion of the 3' untranslated region of β-actin mRNA resulted in the generation of a 297 base pair product predominant only in normal canine myocardium and a 472 base pair product that became increasingly prominent from 1 to 30 days after DC shock damage to the left ventricle and from 10 to 90 days after creation of mitral regurgitation. Northern analysis showed a three-fold increase in β-actin mRNA after either DC shock or creation of mitral regurgitation. Western analysis revealed an early increase in β-actin protein followed by an apparent decrease to below baseline levels. These observations suggest that changes in β-actin mRNA expression accompany the structural alterations that occur in response to myocardial damage. Whether or not the changes in β-actin mRNA expression play a role in mediating these structural alterations remains to be determined.

AB - Beta-actin, a cytoskeletal protein important in the maintenance of cytoarchitecture, has long been thought to be expressed constitutively in myocardial tissue. As such, β-actin mRNA has been used as a control gene in a wide range of experiments. However, we have uncovered consistent changes in β-actin mRNA expression in canine myocardium remodeling as a result of insult to the left ventricle. The experimental canine models used were either DC shock damage to the left ventricle or volume overload resulting from severe mitral regurgitation. The remodeling process in both canine models is characterized by an increase in left ventricular mass. PCR amplification using primers designed to selectively amplify the 3' end and a portion of the 3' untranslated region of β-actin mRNA resulted in the generation of a 297 base pair product predominant only in normal canine myocardium and a 472 base pair product that became increasingly prominent from 1 to 30 days after DC shock damage to the left ventricle and from 10 to 90 days after creation of mitral regurgitation. Northern analysis showed a three-fold increase in β-actin mRNA after either DC shock or creation of mitral regurgitation. Western analysis revealed an early increase in β-actin protein followed by an apparent decrease to below baseline levels. These observations suggest that changes in β-actin mRNA expression accompany the structural alterations that occur in response to myocardial damage. Whether or not the changes in β-actin mRNA expression play a role in mediating these structural alterations remains to be determined.

KW - Canine gene expression

KW - Cytoskeletal protein

KW - DC shock

KW - Mitral regurgitation

KW - Ventricular remodeling

KW - β-actin

UR - http://www.scopus.com/inward/record.url?scp=0029985672&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029985672&partnerID=8YFLogxK

U2 - 10.1006/jmcc.1996.0006

DO - 10.1006/jmcc.1996.0006

M3 - Article

C2 - 8745214

AN - SCOPUS:0029985672

VL - 28

SP - 53

EP - 63

JO - Journal of Molecular and Cellular Cardiology

JF - Journal of Molecular and Cellular Cardiology

SN - 0022-2828

IS - 1

ER -