Imperial College London

ProfessorMichaelSchneider

Faculty of MedicineNational Heart & Lung Institute

Chair in Cardiology
 
 
 
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Contact

 

+44 (0)013 34621727m.d.schneider Website

 
 
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Location

 

ICTEM buildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Black:1991:10.1172/JCI115470,
author = {Black, FM and Packer, SE and Parker, TG and Michael, LH and Roberts, R and Schwartz, RJ and Schneider, MD},
doi = {10.1172/JCI115470},
journal = {J Clin Invest},
pages = {1581--1588},
title = {The vascular smooth muscle alpha-actin gene is reactivated during cardiac hypertrophy provoked by load.},
url = {http://dx.doi.org/10.1172/JCI115470},
volume = {88},
year = {1991}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Cardiac hypertrophy triggered by mechanical load possesses features in common with growth factor signal transduction. A hemodynamic load provokes rapid expression of the growth factor-inducible nuclear oncogene, c-fos, and certain peptide growth factors specifically stimulate the "fetal" cardiac genes associated with hypertrophy, even in the absence of load. These include the gene encoding vascular smooth muscle alpha-actin, the earliest alpha-actin expressed during cardiac myogenesis; however, it is not known whether reactivation of the smooth muscle alpha-actin gene occurs in ventricular hypertrophy. We therefore investigated myocardial expression of the smooth muscle alpha-actin gene after hemodynamic overload. Smooth muscle alpha-actin mRNA was discernible 24 h after coarctation and was persistently expressed for up to 30 d. In hypertrophied hearts, the prevalence of smooth muscle alpha-actin gene induction was 0.909, versus 0.545 for skeletal muscle alpha-actin (P less than 0.05). Ventricular mass after 2 d or more of aortic constriction was more highly correlated with smooth muscle alpha-actin gene activation (r = 0.852; P = 0.0001) than with skeletal muscle alpha-actin (r = 0.532; P = 0.009); P less than 0.0005 for the difference in the correlation coefficients. Thus, smooth muscle alpha-actin is a molecular marker of the presence and extent of pressure-overload hypertrophy, whose correlation with cardiac growth at least equals that of skeletal alpha-actin. Induction of smooth muscle alpha-actin was delayed and sustained after aortic constriction, whereas the nuclear oncogenes c-jun and junB were expressed rapidly and transiently, providing potential dimerization partners for transcriptional control by c-fos.
AU - Black,FM
AU - Packer,SE
AU - Parker,TG
AU - Michael,LH
AU - Roberts,R
AU - Schwartz,RJ
AU - Schneider,MD
DO - 10.1172/JCI115470
EP - 1588
PY - 1991///
SN - 0021-9738
SP - 1581
TI - The vascular smooth muscle alpha-actin gene is reactivated during cardiac hypertrophy provoked by load.
T2 - J Clin Invest
UR - http://dx.doi.org/10.1172/JCI115470
UR - https://www.ncbi.nlm.nih.gov/pubmed/1834699
VL - 88
ER -