ArticleThe Journal of physiology2003
Troponin I in the murine myocardium: influence on length-dependent activation and interfilament spacing.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 1 of them a synthesis that pooled it.
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Who cites it
92 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.
- Implications of S-glutathionylation of sarcomere proteins in cardiac disorders, therapies, and diagnosis.Frontiers in cardiovascular medicine · 2022Pooled it
- Myosin motor dynamics and cardiac function: Insights from in vivo small-angle X-ray scattering and pressure-volume analysis.The Journal of physiology · 2026Article
- Myosin-actin crossbridge independent sarcomere length induced CaJournal of molecular and cellular cardiology · 2025Article
- Abnormal phosphorylation / dephosphorylation and CaHeart failure reviews · 2024Review
- Thin filament regulation of cardiac muscle power output: Implications for targets to improve human failing hearts.The Journal of general physiology · 2023Article
- Sarcomere length affects Ca2+ sensitivity of contraction in ischemic but not non-ischemic myocardium.The Journal of general physiology · 2023Article
- A gradient of force generation at rest differentiates cardiomyopathy outcomes with variants of actin located at the same residue.Journal of molecular and cellular cardiology plus · 2022Article
- Cardiac MyBP-C phosphorylation regulates the Frank-Starling relationship in murine hearts.The Journal of general physiology · 2021Article
- Novel insights into sarcomere regulatory systems control of cardiac thin filament activation.The Journal of general physiology · 2021Article
- Mechanisms of Frank-Starling law of the heart and stretch activation in striated muscles may have a common molecular origin.Journal of muscle research and cell motility · 2021Article
- High efficiency preparation of skinned mouse cardiac muscle strips from cryosections for contractility studies.Experimental physiology · 2020Article
- Hypertrophic and Dilated Cardiomyopathy-Associated Troponin T Mutations R130C and ΔK210 Oppositely Affect Length-Dependent Calcium Sensitivity of Force Generation.Frontiers in physiology · 2020Article
- Increased myocyte calcium sensitivity in end-stage pediatric dilated cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2019Article
- Regulating myofilament power: The determinant of health.Archives of biochemistry and biophysics · 2019Review
- Sarcomere length-dependent effects on CaThe Journal of general physiology · 2019Article
- Cardiac-specific knockout of Lmod2 results in a severe reduction in myofilament force production and rapid cardiac failure.Journal of molecular and cellular cardiology · 2018Article
- The force and stiffness of myosin motors in the isometric twitch of a cardiac trabecula and the effect of the extracellular calcium concentration.The Journal of physiology · 2018Article
- Organ-level right ventricular dysfunction with preserved Frank-Starling mechanism in a mouse model of pulmonary arterial hypertension.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- Altered myofilament structure and function in dogs with Duchenne muscular dystrophy cardiomyopathy.Journal of molecular and cellular cardiology · 2018Article
- The continuing evolution of cardiac troponin I biomarker analysis: from protein to proteoform.Expert review of proteomics · 2017Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Cyclic AMP-dependent protein kinase (PKA) targets contractile proteins, troponin-I (TnI) and myosin binding protein C (MyBP-C) in the heart and induces a decrease in myofilament Ca2+ sensitivity. Yet, the effect of sarcomere length (SL) change on Ca2+ sensitivity (length-dependent activation: LDA) following PKA-dependent phosphorylation is not clear. To clarify the role of PKA-dependent phosphorylation of TnI and MyBP-C on LDA in the heart, we examined LDA in skinned myocytes from a non-transgenic (NTG) and a transgenic murine model in which the native cardiac isoform (cTnI) was completely replaced by the slow skeletal isoform of TnI (ssTnI-TG) lacking the phosphorylation sites for PKA, while retaining PKA sites on MyBP-C. In NTG myocytes, PKA treatment decreased Ca2+ sensitivity at each SL, but enhanced the impact of SL change on Ca2+ sensitivity. Despite a greater sensitivity to Ca2+ and a reduction in LDA, neither Ca2+ responsiveness nor LDA was affected by PKA treatment in ssTnI-TG myocytes. To determine whether the above observations could be explained by the lateral separation between thick and thin filaments, as suggested by others, we measured interfilament spacing by X-ray diffraction as a function of SL in skinned cardiac trabeculae in the passive state from both NTG and ssTnI-TG models before and following treatment with PKA. Phosphorylation by PKA increased lattice spacing at every SL in NTG trabeculae. However, the relationship between SL and myofilament lattice spacing in ssTnI-TG was markedly shifted downward to an overall decreased myofilament lattice spacing following PKA treatment. We conclude: (1) PKA-dependent phosphorylation enhances length-dependent activation in NTG hearts; (2) replacement of native TnI with ssTnI increases Ca2+ sensitivity of tension but reduces length-dependent activation; (3) MyBP-C phosphorylation by PKA does not alter calcium responsiveness and induces a decrease in myofilament lattice spacing at all sarcomere lengths and (4) length-dependent activation in the heart cannot be entirely explained by alterations in myofilament lattice spacing.
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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.