ArticleJournal of molecular and cellular cardiology2010
Stage-specific changes in myofilament protein phosphorylation following myocardial infarction in mice.
Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Intense light as potential future therapy for myocardial injury in patients after non cardiac surgery: lessons from mice and men.Annals of translational medicine · 2025Article
- Housekeeping Proteins Exhibit a High Level of Expression Variability Within Control Group and Between Ischemic Human Heart Biopsies.Journal of the American Heart Association · 2022Article
- Cardiac myosin super relaxation (SRX): a perspective on fundamental biology, human disease and therapeutics.Biology open · 2021Review
- Increased myocyte calcium sensitivity in end-stage pediatric dilated cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2019Article
- Troponin I modulation of cardiac performance: Plasticity in the survival switch.Archives of biochemistry and biophysics · 2019Review
- The continuing evolution of cardiac troponin I biomarker analysis: from protein to proteoform.Expert review of proteomics · 2017Review
- Functional communication between PKC-targeted cardiac troponin I phosphorylation sites.Archives of biochemistry and biophysics · 2017Article
- A post-MI power struggle: adaptations in cardiac power occur at the sarcomere level alongside MyBP-C and RLC phosphorylation.American journal of physiology. Heart and circulatory physiology · 2016Article
- Functionally conservative substitutions at cardiac troponin I S43/45.Archives of biochemistry and biophysics · 2016Article
- Genetic ablation of interleukin-18 does not attenuate hypobaric hypoxia-induced right ventricular hypertrophy.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Mechanisms of favorable effects of Rho kinase inhibition on myocardial remodeling and systolic function after experimental myocardial infarction in the rat.Therapeutic advances in cardiovascular disease · 2016Article
- Independent modulation of contractile performance by cardiac troponin I Ser43 and Ser45 in the dynamic sarcomere.Journal of molecular and cellular cardiology · 2015Article
- Phosphorylation of protein kinase C sites Ser42/44 decreases Ca(2+)-sensitivity and blunts enhanced length-dependent activation in response to protein kinase A in human cardiomyocytes.Archives of biochemistry and biophysics · 2014Article
- The art of the deal in myofilament modulation of function.Journal of molecular and cellular cardiology · 2014Article
- Characterization and validation of new tools for measuring site-specific cardiac troponin I phosphorylation.Journal of immunological methods · 2014Article
- Myofilament calcium de-sensitization and contractile uncoupling prevent pause-triggered ventricular tachycardia in mouse hearts with chronic myocardial infarction.Journal of molecular and cellular cardiology · 2013Article
- Myofilament incorporation and contractile function after gene transfer of cardiac troponin I Ser43/45Ala.Archives of biochemistry and biophysics · 2013Article
- Contractile protein phosphorylation predicts human heart disease phenotypes.American journal of physiology. Heart and circulatory physiology · 2013Article
- Adora2b-elicited Per2 stabilization promotes a HIF-dependent metabolic switch crucial for myocardial adaptation to ischemia.Nature medicine · 2012Article
- Myocardial infarction in mice alters sarcomeric function via post-translational protein modification.Molecular and cellular biochemistry · 2012Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
The response of cardiac muscle to an insult such as myocardial infarction includes changes in the expression of numerous signaling proteins and modulation of gene expression, as well as post-translational modifications of existing proteins. Most studies to date have defined these in end-stage cardiac muscle thus obviating consideration of the temporal progression that causes the heart to transition from a compensated to a decompensated phenotype. To explore these transitions, we examined contractile protein biochemistry in a mouse MI model at two early time points: 2 days and 2 weeks post-infarct and at two later time points: 2 and 4 months post-infarct. Phosphorylation of myofilament proteins was analyzed using phosphospecific staining of polyacrylamide gels, and whenever possible, phosphospecific antibodies. Phosphorylation of myosin binding protein c, the myosin regulatory light chain and troponin I were all decreased relative to sham operated animals at both early time points. However, by 2 months, total phosphorylation of all the major myofilament proteins normalized and at both 2 and 4 months, there was a significant increase in troponin I phosphorylation. One-dimensional IEF of troponin I coupled with phospho-specific antibody analysis demonstrated a redistribution of phosphorylation sites with a significant initial decline at the putative PKA sites, Serine 22,23, and a subsequent increase at the putative PKC site, serine 43,45. These data suggest that temporal changes in myofilament protein phosphorylation contribute both to the initial compensatory hyperdynamic response to myocardial infarction and subsequently to the gradual progression to myocardial failure.
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