scholarly journals Pressure Overload Is Associated With Low Levels of Troponin I and Myosin Binding Protein C Phosphorylation in the Hearts of Patients With Aortic Stenosis

2020 ◽  
Vol 11 ◽  
Author(s):  
O’neal Copeland ◽  
Andrew Messer ◽  
Andrew Jabbour ◽  
Corrado Poggesi ◽  
Sanjay Prasad ◽  
...  
Keyword(s):  
Aortic Stenosis ◽  
Protein C ◽  
Troponin I ◽  
Binding Protein ◽  
Pressure Overload ◽  
Myosin Binding Protein ◽  
Myosin Binding Protein C ◽  
Myosin Binding ◽  
Low Levels

scholarly journals The Interplay between S-glutathionylation and Phosphorylation of Cardiac Troponin I and Myosin Binding Protein C in End-Stage Human Failing Hearts

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1134
Author(s):  
Heidi Budde ◽  
Roua Hassoun ◽  
Melina Tangos ◽  
Saltanat Zhazykbayeva ◽  
Melissa Herwig ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein C ◽  
Troponin I ◽  
Reduced Glutathione ◽  
Binding Protein ◽  
Enzyme Treatment ◽  
Myosin Binding Protein ◽  
Myosin Binding Protein C ◽  
Myosin Binding ◽  
End Stage

Oxidative stress is defined as an imbalance between the antioxidant defense system and the production of reactive oxygen species (ROS). At low levels, ROS are involved in the regulation of redox signaling for cell protection. However, upon chronical increase in oxidative stress, cell damage occurs, due to protein, DNA and lipid oxidation. Here, we investigated the oxidative modifications of myofilament proteins, and their role in modulating cardiomyocyte function in end-stage human failing hearts. We found altered maximum Ca2+-activated tension and Ca2+ sensitivity of force production of skinned single cardiomyocytes in end-stage human failing hearts compared to non-failing hearts, which was corrected upon treatment with reduced glutathione enzyme. This was accompanied by the increased oxidation of troponin I and myosin binding protein C, and decreased levels of protein kinases A (PKA)- and C (PKC)-mediated phosphorylation of both proteins. The Ca2+ sensitivity and maximal tension correlated strongly with the myofilament oxidation levels, hypo-phosphorylation, and oxidative stress parameters that were measured in all the samples. Furthermore, we detected elevated titin-based myocardial stiffness in HF myocytes, which was reversed by PKA and reduced glutathione enzyme treatment. Finally, many oxidative stress and inflammation parameters were significantly elevated in failing hearts compared to non-failing hearts, and corrected upon treatment with the anti-oxidant GSH enzyme. Here, we provide evidence that the altered mechanical properties of failing human cardiomyocytes are partially due to phosphorylation, S-glutathionylation, and the interplay between the two post-translational modifications, which contribute to the development of heart failure.

scholarly journals Roles of phosphorylation of myosin binding protein-C and troponin I in mouse cardiac muscle twitch dynamics

2004 ◽  
Vol 558 (3) ◽  
pp. 927-941 ◽  
Author(s):  
Carl W. Tong ◽  
Robert D. Gaffin ◽  
David C. Zawieja ◽  
Mariappan Muthuchamy
Keyword(s):  
Cardiac Muscle ◽  
Protein C ◽  
Troponin I ◽  
Binding Protein ◽  
Muscle Twitch ◽  
Myosin Binding Protein ◽  
Myosin Binding Protein C ◽  
Myosin Binding

scholarly journals Cardiac Myosin-binding Protein C and Troponin-I Phosphorylation Independently Modulate Myofilament Length-dependent Activation

2015 ◽  
Vol 290 (49) ◽  
pp. 29241-29249 ◽  
Author(s):  
Mohit Kumar ◽  
Suresh Govindan ◽  
Mengjie Zhang ◽  
Ramzi J. Khairallah ◽  
Jody L. Martin ◽  
...  
Keyword(s):  
Protein C ◽  
Troponin I ◽  
Binding Protein ◽  
Cardiac Myosin ◽  
Myosin Binding Protein ◽  
Myosin Binding Protein C ◽  
Myosin Binding ◽  
Length Dependent Activation

scholarly journals 151 Cardiac Myosin-Binding Protein C is a Novel Marker of Myocardial Injury and Fibrosis in Patients with Aortic Stenosis

Heart ◽  
2016 ◽  
Vol 102 (Suppl 6) ◽  
pp. A109.2-A110
Author(s):  
Atul Anand ◽  
Calvin Chin ◽  
Anoop Shah ◽  
Jacek Kwieciński ◽  
Alex Vesey ◽  
...  
Keyword(s):  
Aortic Stenosis ◽  
Protein C ◽  
Myocardial Injury ◽  
Binding Protein ◽  
Cardiac Myosin ◽  
Myosin Binding Protein ◽  
Myosin Binding Protein C ◽  
Myosin Binding
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