ArticleThe Journal of clinical investigation1991
The vascular smooth muscle alpha-actin gene is reactivated during cardiac hypertrophy provoked by load.
Article in The Journal of clinical investigation, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 123 citations in OpenAlex.
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- Induced pluripotent stem cell-derived cardiomyocytes-more show than substance?Biophysical reviews · 2023Review
- Human ApoE2 Endows Stronger Contractility in Rat Cardiomyocytes Enhancing Heart Function.Cells · 2023Article
- Cardiomyocyte maturation: advances in knowledge and implications for regenerative medicine.Nature reviews. Cardiology · 2020Review
- Urocortin 2 Gene Transfer Improves Heart Function in Aged Mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Reactivation of Atrium Genes Is a Primer for Heart Infarction or Regeneration.Frontiers in cardiovascular medicine · 2020Article
- An Improved Method of Maintaining Primary Murine Cardiac Fibroblasts in Two-Dimensional Cell Culture.Scientific reports · 2019Article
- Characterization of cytoskeleton features and maturation status of cultured human iPSC-derived cardiomyocytes.European journal of histochemistry : EJH · 2017Article
- The CSRP2BP histone acetyltransferase drives smooth muscle gene expression.Nucleic acids research · 2017Article
- Cardiac-specific ablation of the E3 ubiquitin ligase Mdm2 leads to oxidative stress, broad mitochondrial deficiency and early death.PloS one · 2017Article
- Myocardial plasticity: cardiac development, regeneration and disease.Current opinion in genetics & development · 2016Review
- Establishment of a prediction model of changing trends in cardiac hypertrophy disease based on microarray data screening.Experimental and therapeutic medicine · 2016Article
- Harnessing fetal and adult genetic reprograming for therapy of heart disease.Journal of nature and science · 2015Article
- Temporal and Molecular Analyses of Cardiac Extracellular Matrix Remodeling following Pressure Overload in Adiponectin Deficient Mice.PloS one · 2015Article
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- Up-regulation of alpha-smooth muscle actin in cardiomyocytes from non-hypertrophic and non-failing transgenic mouse hearts expressing N-terminal truncated cardiac troponin I.FEBS open bio · 2013Article
- Reverse right ventricular structural and extracellular matrix remodeling by estrogen in severe pulmonary hypertension.Journal of applied physiology (Bethesda, Md. : 1985) · 2012Article
- JunB transcription factor maintains skeletal muscle mass and promotes hypertrophy.The Journal of cell biology · 2010Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
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.
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