ArticleThe Journal of biological chemistry2012
Tropomyosin dephosphorylation results in compensated cardiac hypertrophy.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Interventricular Differences of Signaling Pathways-Mediated Regulation of Cardiomyocyte Function in Response to High Oxidative Stress in the Post-Ischemic Failing Rat Heart.Antioxidants (Basel, Switzerland) · 2021Article
- Acidosis modifies effects of phosphorylated tropomyosin on the actin-myosin interaction in the myocardium.Journal of muscle research and cell motility · 2021Article
- Functionally Integrated Top-Down Proteomics for Standardized Assessment of Human Induced Pluripotent Stem Cell-Derived Engineered Cardiac Tissues.Journal of proteome research · 2021Article
- Analysis of fibrosis in control or pressure overloaded rat hearts after mechanical unloading by heterotopic heart transplantation.Scientific reports · 2019Article
- Tropomyosin pseudo-phosphorylation results in dilated cardiomyopathy.The Journal of biological chemistry · 2019Article
- Cardiac Troponin and Tropomyosin: Structural and Cellular Perspectives to Unveil the Hypertrophic Cardiomyopathy Phenotype.Frontiers in physiology · 2016Review
- Phosphorylation of Ser283 enhances the stiffness of the tropomyosin head-to-tail overlap domain.Archives of biochemistry and biophysics · 2015Article
- Top-down mass spectrometry of cardiac myofilament proteins in health and disease.Proteomics. Clinical applications · 2014Review
- Decreasing tropomyosin phosphorylation rescues tropomyosin-induced familial hypertrophic cardiomyopathy.The Journal of biological chemistry · 2013Article
- The β-arrestin-biased ligand TRV120023 inhibits angiotensin II-induced cardiac hypertrophy while preserving enhanced myofilament response to calcium.American journal of physiology. Heart and circulatory physiology · 2013Article
- Alpha-tropomyosin mutations in inherited cardiomyopathies.Journal of muscle research and cell motility · 2013Review
- Phosphorylation of tropomyosin in striated muscle.Journal of muscle research and cell motility · 2013Review
- Tropomyosin de-phosphorylation in the heart: what are the consequences?Journal of muscle research and cell motility · 2013Review
- Tropomyosin isoform expression and phosphorylation in the human heart in health and disease.Journal of muscle research and cell motility · 2013Article
- A study of tropomyosin's role in cardiac function and disease using thin-filament reconstituted myocardium.Journal of muscle research and cell motility · 2013Review
- Conserved Asp-137 is important for both structure and regulatory functions of cardiac α-tropomyosin (α-TM) in a novel transgenic mouse model expressing α-TM-D137L.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Phosphorylation of tropomyosin (Tm) has been shown to vary in mouse models of cardiac hypertrophy. Little is known about the in vivo role of Tm phosphorylation. This study examines the consequences of Tm dephosphorylation in the murine heart. Transgenic (TG) mice were generated with cardiac specific expression of α-Tm with serine 283, the phosphorylation site of Tm, mutated to alanine. Echocardiographic analysis and cardiomyocyte cross-sectional area measurements show that α-Tm S283A TG mice exhibit a hypertrophic phenotype at basal levels. Interestingly, there are no alterations in cardiac function, myofilament calcium (Ca(2+)) sensitivity, cooperativity, or response to β-adrenergic stimulus. Studies of Ca(2+) handling proteins show significant increases in sarcoplasmic reticulum ATPase (SERCA2a) protein expression and an increase in phospholamban phosphorylation at serine 16, similar to hearts under exercise training. Compared with controls, the decrease in phosphorylation of α-Tm results in greater functional defects in TG animals stressed by transaortic constriction to induce pressure overload-hypertrophy. This is the first study to investigate the in vivo role of Tm dephosphorylation under both normal and cardiac stress conditions, documenting a role for Tm dephosphorylation in the maintenance of a compensated or physiological phenotype. Collectively, these results suggest that modification of the Tm phosphorylation status in the heart, depending upon the cardiac state/condition, may modulate the development of cardiac hypertrophy.
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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.