ArticleProceedings of the National Academy of Sciences of the United States of America2008
Discordant on/off switching of gene expression in myocytes during cardiac hypertrophy in vivo.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Trial
- Stromal Cell-SLIT3/Cardiomyocyte-ROBO1 Axis Regulates Pressure Overload-Induced Cardiac Hypertrophy.Circulation research · 2024Article
- The lack of Troponin I Ser-23/24 phosphorylation is detrimental to in vivo cardiac function and exacerbates cardiac disease.Journal of molecular and cellular cardiology · 2023Article
- GRK5-mediated inflammation and fibrosis exert cardioprotective effects during the acute phase of myocardial infarction.FEBS open bio · 2023Article
- Article
- Cardiac Myosin Heavy Chain Reporter Mice to Study Heart Development and Disease.Circulation research · 2022Article
- Glucosylceramide synthase inhibition protects against cardiac hypertrophy in chronic kidney disease.Scientific reports · 2022Article
- Review
- Role of Mononuclear Cardiomyocytes in Cardiac Turnover and Regeneration.Current cardiology reports · 2020Review
- Novel large-particle FACS purification of adult ventricular myocytes reveals accumulation of myosin and actin disproportionate to cell size and proteome in normal post-weaning development.Journal of molecular and cellular cardiology · 2017Article
- Article
- Small dedifferentiated cardiomyocytes bordering on microdomains of fibrosis: evidence for reverse remodeling with assisted recovery.Journal of cardiovascular pharmacology · 2014Article
- Normal cardiac function in mice with supraphysiological cardiac creatine levels.American journal of physiology. Heart and circulatory physiology · 2014Article
- Getting to the heart of the matter: long non-coding RNAs in cardiac development and disease.The EMBO journal · 2013Review
- β-myosin heavy chain is induced by pressure overload in a minor subpopulation of smaller mouse cardiac myocytes.Circulation research · 2011Article
- Article
- Reversible epigenetic modifications of the two cardiac myosin heavy chain genes during changes in expression.Gene expression · 2010Article
- Decreased beta-adrenergic responsiveness following hypertrophy occurs only in cardiomyocytes that also re-express beta-myosin heavy chain.European journal of heart failure · 2009Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
To determine whether the expression of cardiac genes changes in a graded manner or by on/off switching when cardiac myocytes change genetic programs in living animals, we have studied two indicator genes that change their expression oppositely in mouse binucleate ventricular cardiomyocytes during development and in response to cardiac hypertrophy. One is a single-copy transgene controlled by an alpha-myosin heavy chain (aMHC) promoter and coding for CFP. The other is the endogenous beta-myosin heavy chain (bMHC) gene modified to code for a YFP-bMHC fusion protein. Using high-resolution confocal microscopy, we determined the expression of the two indicator genes in individual cardiomyocytes perinatally and after inducing cardiac hypertrophy by transverse aortic constriction. Our results provide strong evidence that the cardiac genes respond by switching their expression in an on/off rather than graded manner, and that responding genes within a single cell and within the two nuclei of cardiomyocytes do not necessarily switch concordantly.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.