ArticleJournal of molecular and cellular cardiology2008
Selective translation of mRNAs in the left ventricular myocardium of the mouse in response to acute pressure overload.
Article in Journal of molecular and cellular cardiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Regulation of Protein Synthesis at the Translational Level: Novel Findings in Cardiovascular Biology.Biomolecules · 2025Review
- Translational control of Ybx1 expression regulates cardiac function in response to pressure overload in vivo.Basic research in cardiology · 2023Article
- Translating Translation to Mechanisms of Cardiac Hypertrophy.Journal of cardiovascular development and disease · 2020Review
- Article
- FGF2 modulates cardiac remodeling in an isoform- and sex-specific manner.Physiological reports · 2013Article
- Article
- Heat stress in rat adriamycin cardiomyopathy: heat shock protein 25 and Myosin accumulation.Journal of toxicologic pathology · 2010Article
- Immediate response of myocardium to pressure overload includes transient regulation of genes associated with mitochondrial bioenergetics and calcium availability.Genetics and molecular biology · 2010Article
- Beta3 integrin-mediated ubiquitination activates survival signaling during myocardial hypertrophy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009Article
- Integration of Insulin receptor/Foxo signaling and dMyc activity during muscle growth regulates body size in Drosophila.Development (Cambridge, England) · 2009Article
- Biological functions of the low and high molecular weight protein isoforms of fibroblast growth factor-2 in cardiovascular development and disease.Developmental dynamics : an official publication of the American Association of Anatomists · 2009Review
- Phosphorylation of the translation initiation factor eIF2alpha increases BACE1 levels and promotes amyloidogenesis.Neuron · 2008Article
- Protein quality control and degradation in cardiomyocytes.Journal of molecular and cellular cardiology · 2008Review
- The ins and outs of calcium in heart failure.Circulation research · 2008Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
During pressure overload hypertrophy, selective changes in cardiac gene expression occur that regulate growth and modify the structural and functional properties of the myocardium. To determine the role of translational mechanisms, a murine model of transverse aortic constriction was used to screen a set of specified mRNAs for changes in translational activity by measuring incorporation into polysomes in response to acute pressure overload. Candidate mRNAs were selected on the basis of two main criteria: (1) the 5'-untranslated region of the mRNA contains an excessive amount of secondary structure (DeltaG<-50 kCal/mol), which is postulated to regulate efficiency of translation, and (2) the protein product has been implicated in the regulation of cardiac hypertrophy. After 24 h of transverse aortic constriction, homogenates derived from the left ventricle were layered onto 15-50% linear sucrose gradients and resolved into monosome fractions (messenger ribonucleoprotein particles) and polysome fractions by density gradient ultracentrifugation. The levels of mRNA in each fraction were quantified by real-time RT-PCR. The screen revealed that pressure overload increased translational activity of 6 candidate mRNAs as determined by a significant increase in the percentage of total mRNA incorporated into the polysome fractions. The mRNAs code for several functional classes of proteins linked to cardiac hypertrophy: the transcription factors c-myc, c-jun and MEF2D, growth factors VEGF and FGF-2 and the E3 ubiquitin ligase MDM2. These studies demonstrate that acute pressure overload alters cardiac gene expression by mechanisms that selectively regulate translational activity of specific mRNAs.
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