University of Kentucky

Poster Title

STUDY 2: PKC-Dependent Phosphorylation of Cardiac Troponin T

Institution

University of Kentucky

Abstract

Heart failure is the leading cause of death in the United States. According to the Heart Failure Society of America, an estimated 400,000 to 700,000 new cases of heart failure are diagnosed each year. Heart disease is the number one killer in Kentucky; over 12,000 people in Kentucky died of heart disease in 2000. Hypertension, diabetes, and missense mutations often lead to heart failure. When heart performance is affected by such conditions, the heart responds by increasing myocyte (heart cell) size and cause a greater volume of blood to go through the heart (chamber dilation). This compensatory mechanism is collectively termed, “remodeling”; the remodeling process works to preserve pump function in disease state. Although cardiac remodeling can initially be beneficial to heart function, it can eventually become maladaptive, and ultimately lead to heart failure. Mounting evidence supports the overall hypothesis that troponin phosphorylation is a key mechanism involved in the contractile dysfunction associated with heart failure. Phosphorylation of thin-filament regulatory proteins cardiac troponin I (cTnI) and troponin T (cTnT) is known to depress muscle fiber ATP consumption rate and force generation. Our long-term goal is to elucidate signal transduction and cellular and molecular mechanisms by which phosphorylation of troponin leads to alterations in cardiac muscle function and ultimately to heart failure and to identify new therapeutical targets.

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STUDY 2: PKC-Dependent Phosphorylation of Cardiac Troponin T

Heart failure is the leading cause of death in the United States. According to the Heart Failure Society of America, an estimated 400,000 to 700,000 new cases of heart failure are diagnosed each year. Heart disease is the number one killer in Kentucky; over 12,000 people in Kentucky died of heart disease in 2000. Hypertension, diabetes, and missense mutations often lead to heart failure. When heart performance is affected by such conditions, the heart responds by increasing myocyte (heart cell) size and cause a greater volume of blood to go through the heart (chamber dilation). This compensatory mechanism is collectively termed, “remodeling”; the remodeling process works to preserve pump function in disease state. Although cardiac remodeling can initially be beneficial to heart function, it can eventually become maladaptive, and ultimately lead to heart failure. Mounting evidence supports the overall hypothesis that troponin phosphorylation is a key mechanism involved in the contractile dysfunction associated with heart failure. Phosphorylation of thin-filament regulatory proteins cardiac troponin I (cTnI) and troponin T (cTnT) is known to depress muscle fiber ATP consumption rate and force generation. Our long-term goal is to elucidate signal transduction and cellular and molecular mechanisms by which phosphorylation of troponin leads to alterations in cardiac muscle function and ultimately to heart failure and to identify new therapeutical targets.