Troponin I is part of a heteromeric thin filament regulatory complex that governs skeletal and cardiac muscle contraction. Troponin I is composed of three subunits: troponin I (TnI), troponin T (TnT), and troponin C (TnC), and each of these components plays a different functional role. For example, TnI is an inhibitory component, and confers calcium-sensitivity to the ATPase activity of the myofibril contractile apparatus within striated muscles. Through blocking actin-myosin interactions, TnI modulates muscle relaxation. TnI itself is actually encoded by three different genes which produce tissue-specific isoforms as follows: TnI Type 1 (skeletal-slow-twitch), TnI Type 2 (skeletal-fast-twitch), and TnI Type 3 (cardiac). As their nomenclature implies, TnI Types 1 and 2 are expressed solely in fast- or slow-twitch skeletal muscle fibers, respectively. TnI Type 3 is exclusively found expressed in the myocardium of cardiac muscle tissue. Because it is unlike other contractile proteins in that it is expressed only in cardiac muscle, TnI Type 3 is an ideal cardiac-specific expression marker.
It is also elevated in severe heart failure, also making it a sensitive and specific indicator for myocardial cell injury, and therefore useful in the diagnosis and assessment of acute coronary disease. Additionally, TnI Type 3 exhibits a developmental regulation pattern that includes increased expression at the time of birth. Chang et al share a concise summary of various dilated cardiomyopathy (DCM)-associated mutations found in a wide range of sarcomere and cytoskeleton proteins (beta-myosin heavy chain, actin, TnI, TnT, TnC, desmin, and vinculin) using a Troponin I type 3 antibody (1). A very recent comprehensive study from Vorovich's group at the U Penn School of Medicine evaluated 9 biomarkers as predictors of cardiac hospitalization in cases of chronic heart failure (HF), and found that B-type natriuretic peptide and troponin I demonstrated the strongest association via utilization of a Troponin I type 3 antibody (2). Furthermore, Hsu’s group at the National Cheng Kung University in Taiwan used the Troponin I type 3 antibody in both immunohistochemical and immunofluorescence studies on the ECM protein CCN1 (3). Their data establishes CCN1 as a crucial pathophysiological regular of apoptosis in response to injury.
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