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Cardiac troponin T composition in normal and regenerating human skeletal muscle
G S Bodor1, L Survant, E M Voss
1Department of Pathology, Vanderbilt University School of Medicine, Nashville, TN 37232-5310, USA. bodorgs@ctrvax.vanderbilt.edu
Insights
Cardiac troponin T (cTnT) is not exclusively found in the heart. This study found cTnT in normal and diseased human skeletal muscle, challenging its cardiac specificity and impacting diagnostic interpretations.
Area of Science:
- Biochemistry
- Molecular Biology
- Cardiology
Background:
- Cardiac troponin T (cTnT) is a key biomarker for diagnosing myocardial infarction.
- Previous studies suggested cTnT is exclusively present in cardiac tissue.
- Recent findings indicate cTnT presence in non-cardiac conditions, prompting further investigation.
Purpose of the Study:
- To investigate the presence and expression levels of cTnT in human skeletal muscle tissues.
- To determine if cTnT is exclusively cardiac-specific.
- To compare cTnT expression in normal, polymyositis (PM), and Duchenne muscular dystrophy (DMD) skeletal muscle.
Main Methods:
- Immunohistochemistry was used to detect cTnT in tissue samples.
- Western blot analysis confirmed cTnT expression.
- Quantitative cTnT ELISA measured cTnT concentrations in myofibrillar protein.
Main Results:
- cTnT was detected in all heart specimens.
- Skeletal muscle samples showed variable cTnT expression, from none to 20% of fibers.
- cTnT was found in 8/13 PM patients and all 6/6 DMD patients.
- Mean cTnT concentrations were significantly lower in normal skeletal muscle (0.8 mg/g) compared to cardiac muscle (10.0 mg/g) and DMD skeletal muscle (4.37 mg/g).
Conclusions:
- Cardiac troponin T (cTnT) is not 100% cardiac-specific.
- cTnT is expressed in normal human skeletal muscle, with variable levels.
- cTnT is present in regenerating skeletal muscle associated with polymyositis and Duchenne muscular dystrophy.
- These findings necessitate a re-evaluation of cTnT's role as a purely cardiac biomarker.
Abstract:
Cardiac troponin T (cTnT), measurement of which has been recommended for diagnosing myocardial infarction, was initially believed to be specific for the heart. However, recent publications have reported cTnT in sera of patients without cardiac disease; therefore, we investigated whether cTnT could be found in human skeletal muscle tissues. Using immunohistochemistry, Western blot, and quantitative cTnT ELISA, we assayed human heart (n = 3), normal human skeletal muscle (n = 6), and diseased skeletal muscle samples from patients with polymyositis (PM, n = 13) and Duchenne muscular dystrophy (DMD, n = 6). All heart specimens contained cTnT, but the expression of cTnT in normal skeletal muscle samples varied widely, ranging from no expression (quadriceps femoris) to expression by up to 20% of the muscle fibers (diaphragm). Immunohistochemistry detected cTnT in skeletal muscle of 8 of the PM patients and all of the DMD patients. Mean myofibrillar cTnT concentrations (mg/g myofibrillar protein) were: cardiac = 10.0, normal skeletal = 0.8, PM skeletal = 0.7, and DMD skeletal = 4.37, confirming the results of immunohistochemistry. Western blot analysis also confirmed the expression of cTnT in muscle from DMD patients. These findings provide evidence that cTnT is not 100% cardiac-specific but also is expressed in regenerating (PM and DMD) as well as in normal (nonregenerating) skeletal muscle.