ArticleAmerican journal of physiology. Heart and circulatory physiology2010
H2O2 alters rat cardiac sarcomere function and protein phosphorylation through redox signaling.
Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Mitochondrial Dysfunction in HFpEF: Potential Interventions Through Exercise.Journal of cardiovascular translational research · 2025Review
- Oxidative stress initiates hemodynamic change in CKD-induced heart disease.Basic research in cardiology · 2024Article
- Long-Term PDE-5A Inhibition Improves Myofilament Function in Left and Right Ventricular Cardiomyocytes through Partially Different Mechanisms in Diabetic Rat Hearts.Antioxidants (Basel, Switzerland) · 2021Article
- Screening forTheranostics · 2020Article
- Mitochondrial oxidative stress impairs contractile function but paradoxically increases muscle mass via fibre branching.Journal of cachexia, sarcopenia and muscle · 2019Article
- Estrogen but not testosterone preserves myofilament function from doxorubicin-induced cardiotoxicity by reducing oxidative modifications.American journal of physiology. Heart and circulatory physiology · 2019Article
- Deliberate ROS production and auxin synergistically trigger the asymmetrical division generating the subsidiary cells in Zea mays stomatal complexes.Protoplasma · 2016Article
- Mechanotransduction and Metabolism in Cardiomyocyte Microdomains.BioMed research international · 2016Review
- Myocardial creatine levels do not influence response to acute oxidative stress in isolated perfused heart.PloS one · 2014Article
- Integration of troponin I phosphorylation with cardiac regulatory networks.Circulation research · 2013Review
- Alteration of energy substrates and ROS production in diabetic cardiomyopathy.Mediators of inflammation · 2013Review
- Modulation of K2P3.1 (TASK-1), K2P9.1 (TASK-3), and TASK-1/3 heteromer by reactive oxygen species.Pflugers Archiv : European journal of physiology · 2012Article
- Impact of hydroxyl radical-induced injury on calcium handling and myofilament sensitivity in isolated myocardium.Journal of applied physiology (Bethesda, Md. : 1985) · 2012Article
- Sphingomyelinase depresses force and calcium sensitivity of the contractile apparatus in mouse diaphragm muscle fibers.Journal of applied physiology (Bethesda, Md. : 1985) · 2012Article
- Chemotherapy-induced weakness and fatigue in skeletal muscle: the role of oxidative stress.Antioxidants & redox signaling · 2011Review
- Mechanics on myocardium deficient in the N2B region of titin: the cardiac-unique spring element improves efficiency of the cardiac cycle.Biophysical journal · 2011Article
- Redox signaling in cardiac myocytes.Free radical biology & medicine · 2011Review
- Redox signaling and cardiac sarcomeres.The Journal of biological chemistry · 2011Review
- Novel function of cardiac protein kinase D1 as a dynamic regulator of Ca2+ sensitivity of contraction.The Journal of biological chemistry · 2010Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
ROS, such as H(2)O(2), are a component of pathological conditions in many organ systems and have been reported to be elevated in cardiac pathophysiology. The experiments presented here test the hypothesis that H(2)O(2) induces alterations in cardiac myofilament function by the posttranslational modification of sarcomeric proteins indirectly through PKC signaling. In vitro assessment of actomyosin Mg(2+)-ATPase activity of myofibrillar fractions showed blunted relative ATP consumption in the relaxed state (pCa 8.0) in response to treatment with 0.5 mM H(2)O(2) before myofilament isolation. The effect was attributable to downstream "redox signaling," inasmuch as the direct application of H(2)O(2) to isolated myofibrils did not alter Mg(2+)-ATPase activity. Ca(2+)-ATPase activity, which was used as a measure of myofibrillar myosin function, was unaffected by H(2)O(2). Functional experiments using rat cardiac trabeculae treated with 0.5 or 5 mM H(2)O(2) followed by detergent extraction of membranes demonstrated increased Ca(2+) sensitivity of force production, a faster rate of force redevelopment, and (for 5 mM) decreased maximum tension. Biochemical analysis of myocardial samples treated with 0.5 mM H(2)O(2) demonstrated increased phosphorylation of two sarcomeric proteins: cardiac troponin I and myosin-binding protein-C. These changes were eliminated by a general PKC inhibitor. However, H(2)O(2) and the general PKC activator PMA induced different phosphorylation patterns in cardiomyocytes in which PKC-delta was elevated by viral infection. These data provide evidence that PKC-dependent redox signaling affects the function of cardiac myofilaments and indicate modification of specific proteins through this signaling mechanism.
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