Cardiac troponin-I is not expressed in fetal and healthy or diseased adult human skeletal muscle tissue

Abstract

Cardiac troponin-I (cTnI) is not found in sera of patients with skeletal muscle disease in the absence of myocardial injury. It is not known, however, whether trace amounts of cTnI are expressed in regenerating human skeletal muscle, as has been observed with creatine kinase MB. Using immunohistochemical and biochemical techniques, we investigated cTnI expression in various human muscle tissues: human heart tissue (n = 5), normal adult skeletal muscle (n = 3), and fetal heart (n = 3) and skeletal muscle (n = 3) obtained, respectively, during heart transplant, from autopsy, or from a tissue bank. Specimens from diagnostic tissue biopsies were used as diseased skeletal muscle: polymyositis (PM), n = 13; Duchenne muscular dystrophy (DMD), n = 6. Frozen sections 8 microns thick were stained immunohistochemically for either cTnI or TnI (cardiac or skeletal) by using monoclonal antibodies (MAb) 2B1.9 (cTnI specific) or 3C5.10 (reactive with all TnI isoforms), respectively. cTnI was measured in tissue homogenates by an immunofluorometric assay. Cardiac muscle was stained by both MAbs. Normal fetal and adult skeletal muscle, and samples from all of the PM and DMD patients, stained only with the nonspecific MAb (3C5.10), confirming the sole presence of skeletal TnI. No cTnI was detectable by immunoassay in any skeletal muscle sample. We conclude that cTnI is not expressed in human skeletal muscle during development or during regenerative muscle disease processes such as PM or DMD.

Prospective Clinical Evaluation of Serum Cardiac Troponin T in Dogs Admitted to a Veterinary Teaching Hospital

“…23,24 CTnI appears to be more specific than cTnT for myocardial injury. 25 Possible increases in serum cTnT concentration with skeletal muscle trauma may be one disadvantage of cTnT compared to cTnI. 2nd-generation cTnT assays (such as the Elecsys used in this study) are reported to be more specific for myocardial injury than 1st-generation assays.…”

“…cTnI has been shown to be a more sensitive and specific marker of myocardial injury. 4,21,[23][24][25] However, some normal dogs may experience slight increases in cTnI, which may cause difficulty in assessing a clinically relevant increase in concentration. 21 Finally, the lack of standardization among the different assays for cTnT and cTnI may be problematic for its widespread clinical use.…”

Increased plasma cardiac troponin I concentration in lambs with myocarditis

“…4 Among the cardiac troponins, cTnI is more specific than cTnT in detecting myocardial damage because cTnT may be expressed by skeletal muscle in human patients with renal failure and muscular dystrophy. 1,25,[27][28][29][30] In this study, plasma cTnI concentrations were measured using the assay developed for use in people, because no sheep-specific assay is available. cTnI is measured by automated immunoassay, and the difference in amino acid sequence between skeletal and cardiac muscle troponin I has permitted production of antibodies specific for cTnI.…”

Cardiac Troponins in Dogs and Cats

“…10,11 It is not expressed in skeletal muscle during disease states and is, thus, uniquely cardiac. [14][15][16] The full gene sequence of cTnI in dogs and cats has been determined, and the homology between canine/feline and human cTnI genes is 95 and 96%. 17 As the troponins are purely intracellular proteins, their presence in circulation reflects intracellular content release from cardiomyocytes.…”