Cardiac troponin T and autoimmunity in skeletal muscle aging

GeroScience ◽  
2022 ◽  
Author(s):  
Tan Zhang ◽  
Xin Feng ◽  
Juan Dong ◽  
Zherong Xu ◽  
Bo Feng ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Cardiac Troponin T ◽  
Muscle Aging ◽  
Skeletal Muscle Aging

scholarly journals Cardiac troponin I, cardiac troponin T, and creatine kinase MB in dialysis patients without ischemic heart disease: evidence of cardiac troponin T expression in skeletal muscle

1997 ◽  
Vol 43 (6) ◽  
pp. 976-982 ◽  
Author(s):  
Mary D McLaurin ◽  
Fred S Apple ◽  
Ellen M Voss ◽  
Charles A Herzog ◽  
Scott W Sharkey
Keyword(s):  
Skeletal Muscle ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Cardiac Troponin ◽  
First Generation ◽  
Troponin T ◽  
Ischemic Heart ◽  
Cardiac Troponin T ◽  
Dialysis Patients ◽  
Acute Ischemic Heart Disease

Abstract Serum cardiac troponin T (cTnT) concentrations are frequently increased in chronic dialysis patients as measured by the first-generation ELISA immunoassay, as is creatine kinase (CK) MB mass in the absence of acute ischemic heart disease. We designed this study to compare four serum markers of myocardial injury [CK-MB mass, first-generation ELISA cTnT, second-generation Enzymun cTnT, and cardiac troponin I (cTnI)] in dialysis patients without acute ischemic heart disease. We also evaluated skeletal muscle from dialysis patients as a potential source of serum cTnT. No patients in the clinical evaluation group (n = 24) studied by history and by physical examination, electrocardiography, and two-dimensional echocardiography had evidence of ischemic heart disease. Biochemical markers were measured in serial predialysis blood samples with specific monoclonal antibody-based immunoassays. For several patients at least one sample measured above the upper reference limit: CK-MB, 7 of 24 (30%); ELISA cTnT, 17 of 24 (71%); Enzymun cTnT, 3 of 18 (17%); and cTnI, 1 of 24 (4%). In a separate group of dialysis patients (n = 5), expression of cTnT, but not cTnI, was demonstrated by Western blot analysis in 4 of 5 skeletal muscle biopsies. Chronic dialysis patients without acute ischemic heart disease frequently had increased serum CK-MB and cTnT. The specificity of the second-generation cTnT (Enzymun) assay was improved over that of the first-generation (ELISA) assay; cTnI was the most specific of the currently available biochemical markers. cTnT, but not cTnI, was expressed in the skeletal muscle of dialysis patients.

scholarly journals Multicenter evaluation of a second-generation assay for cardiac troponin T

1997 ◽  
Vol 43 (10) ◽  
pp. 1877-1884 ◽  
Author(s):  
Hannsjörg Baum ◽  
Siegmund Braun ◽  
Willie Gerhardt ◽  
Georges Gilson ◽  
Gerd Hafner ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Troponin ◽  
First Generation ◽  
Second Generation ◽  
Troponin T ◽  
Myocardial Damage ◽  
Cross Reactivity ◽  
Cardiac Troponin T ◽  
Marathon Runners ◽  
Assay Time

Abstract We report on the evaluation of the second-generation assay for cardiac troponin T (cTnT) on the Enzymun®system. This new assay is completely specific for the cardiac isoform of TnT, utilizing two cardiospecific monoclonal antibodies. The assay time is reduced to 45 min. The interassay precision shows a median CV of 5.5%; 20% interassay CV was found between 0.05 and 0.1 μg/L. The cardiosensitivity of the second-generation cTnT assay in patients with ischemic myocardial injury appears equivalent when compared with the first-generation assay. We found no falsely positive results in patients with skeletal muscle damage including multitraumas, surgery patients, and marathon runners who showed highly increased values with the unspecific first-generation assay. In Duchenne disease cTnT was still increased, but to a much lower extent. cTnT remains increased in renal failure, but to a lesser degree than with the first-generation assay. The cause of this increase remains unclear. Although a cross-reactivity of skeletal muscle TnT in the second-generation assay could be excluded by our findings, minor myocardial damage or expression of the cardiac isoform of TnT in regenerating muscles cannot be ruled out in those cases with apparently falsely increased cTnT values. The second-generation cTnT assay is a step forward in the combination of cardiosensitivity and cardiospecificity in biochemical markers for diagnosis of heart disease.

Effects of exercise on plasma myosin heavy chain fragments and MRI of skeletal muscle

1992 ◽  
Vol 72 (2) ◽  
pp. 656-663 ◽  
Author(s):  
J. Mair ◽  
A. Koller ◽  
E. Artner-Dworzak ◽  
C. Haid ◽  
K. Wicke ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Plasma Concentrations ◽  
Eccentric Contractions ◽  
Cardiac Troponin T ◽  
Skeletal Muscle Myosin ◽  
Slow Skeletal Muscle ◽  
Slow Twitch ◽  
Muscle Myosin

The effects of a single series of high-force eccentric contractions involving the quadriceps muscle group (single leg) on plasma concentrations of muscle proteins were examined as a function of time, in the context of measurements of torque production and magnetic resonance imaging (MRI) of the involved muscle groups. Plasma concentrations of slow-twitch skeletal (cardiac beta-type) myosin heavy chain (MHC) fragments, myoglobin, creatine kinase (CK), and cardiac troponin T were measured in blood samples of six healthy male volunteers before and 2 h after 70 eccentric contractions of the quadriceps femoris muscle. Screenings were conducted 1, 2, 3, 6, 9, and 13 days later. To visualize muscle injury, MRI of the loaded and unloaded thighs was performed 3, 6, and 9 days after the eccentric exercise bout. Force generation of the knee extensors was monitored on a dynamometer (Cybex II+) parallel to blood sampling. Exercise resulted in a biphasic myoglobin release profile, delayed CK and MHC peaks. Increased MHC fragment concentrations of slow skeletal muscle myosin occurred in late samples of all participants, which indicated a degradation of slow skeletal muscle myosin. Because cardiac troponin T was within the normal range in all samples, which excluded a protein release from the heart (cardiac beta-type MHC), this finding provides evidence for an injury of slow-twitch skeletal muscle fibers in response to eccentric contractions. Muscle action revealed delayed reversible increases in MRI signal intensities on T2-weighted images of the loaded vastus intermedius and deep parts of the vastus lateralis. We attributed MRI signal changes due to edema in part to slow skeletal muscle fiber injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of denervation on the content of cardiac troponin-T and cardiac troponin-I in rat skeletal muscle

2007 ◽  
Vol 40 (5-6) ◽  
pp. 423-426 ◽  
Author(s):  
Salim Fredericks ◽  
Hans Degens ◽  
Godfrina McKoy ◽  
Katie Bainbridge ◽  
Paul O. Collinson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Cardiac Troponin I ◽  
Cardiac Troponin T ◽  
Rat Skeletal Muscle

Differential reactivity of cardiac and skeletal muscle from various species in two generations of cardiac troponin-T immunoassays

1998 ◽  
Vol 65 (2) ◽  
pp. 135-137 ◽  
Author(s):  
Peter James O'Brien ◽  
Gregory W. Dameron ◽  
Mary Lee Beck ◽  
Marilyn Brandt
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Cardiac Troponin T ◽  
Differential Reactivity ◽  
Two Generations

scholarly journals Skeletal Muscle Disease as Noncardiac Cause of Cardiac Troponin T Elevation

2012 ◽  
Vol 59 (14) ◽  
pp. 1334-1335 ◽  
Author(s):  
Kosit Sribhen ◽  
Rewat Phankingthongkum ◽  
Nilrat Wannasilp
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Muscle Disease ◽  
Cardiac Troponin T

Cardiac troponin T content in heart and skeletal muscle and in blood samples from ApoE/LDL receptor double knockout mice

2004 ◽  
Vol 344 (1-2) ◽  
pp. 73-78 ◽  
Author(s):  
Christian Löwbeer ◽  
Ann-Marie Forsberg ◽  
Shinichi Tokuno ◽  
Anne-Louise Hemdahl ◽  
Sven A Gustafsson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Knockout Mice ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Ldl Receptor ◽  
Cardiac Troponin T ◽  
Double Knockout ◽  
Blood Samples

scholarly journals Cardiac troponin T isoforms expressed in renal diseased skeletal muscle will not cause false-positive results by the second generation cardiac troponin T assay by Boehringer Mannheim

1998 ◽  
Vol 44 (9) ◽  
pp. 1919-1924 ◽  
Author(s):  
Vincent Ricchiuti ◽  
Ellen M Voss ◽  
Arthur Ney ◽  
Mark Odland ◽  
Page A W Anderson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Molecular Mass ◽  
Cardiac Troponin ◽  
Second Generation ◽  
Troponin T ◽  
Chronic Renal Disease ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Cardiac Troponin T ◽  
Muscle Biopsies

Abstract The purpose of this study was to determine whether the two monoclonal anti-cardiac troponin T (cTnT) antibodies (MAbs) used in the second generation cTnT assay by Boehringer Mannheim (BM, capture Ab, M11.7; detection Ab, M7) would detect cTnT isoforms expressed in human skeletal muscle in response to chronic renal disease (CRD). cTnT expression was examined in skeletal muscle biopsies obtained from 45 CRD patients, as well as nondiseased human heart (n = 3) and skeletal muscle (n = 3). cTnT proteins were resolved by modified 7.5% sodium dodecyl sulfate-polyacrylamide gel electrophoresis, transferred to nitrocellulose, and probed with the following anti-cTnT MAbs: M11.7; M7; JS-2, Lakeland Biomedical; and 13–11, Duke University. All four antibodies detected the cTnT isoforms (Ta, Te) expressed in human myocardium. In 20 of 45 skeletal muscle biopsies, MAb M11.7 recognized its epitope in one to three proteins, molecular mass 34–36 kDa, designated Te, Td, and Tc; the strongest signal was that of Te. The same proteins were recognized by MAbs JS-2 and 13–11. The BM M7 antibody did not detect the cTnT isoforms in the molecular mass range of 34–36 kDa. However, MAb M7 did detect a cTnT isoform, molecular mass 39 kDa, in 2 of 45 biopsies. This isoform had an electrophoretic mobility similar to the predominant heart cTnT isoform, Ta. We conclude that cTnT isoforms are expressed in the skeletal muscle of CRD patients. However, given the epitopes recognized by the BM MAbs M7 and M11.7 and the variable presence of these cTnT isoforms in skeletal muscle, the second generation BM cTnT assay will not detect these isoforms if they are released from skeletal muscle into the circulation.

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