Proteolysis of myosin and troponin in human myocardium of elderly subjects.

Yoshida, Kenichi; Hanafusa, Terukiyo; Matoba, Ryoji; Wakasugi, Choei

doi:10.1536/ihj.31.683

Cited by 7 publications

(3 citation statements)

References 29 publications

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“…Venous blood samples of 10 mL were obtained just before starting thrombolytic therapy and 1,2,3,4, 5,6,8,10,14,18,22,28,34,46,58,70,82,94,118,142, 166 h later. Exact sampling times were recorded and expressed as time after the onset of symptoms.…”

Section: Cardiac Troponin T Release 31s Patients and Memodsmentioning

confidence: 99%

Cardiac Troponin T Release into Plasma after Acute Myocardial Infarction: Only Fractional Recovery Compared with Enzymes

1996

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SUMMARY. After acute myocardial infarction (AMI) cardiac enzymes and proteins are released into plasma and are used as biochemical markers of cardiac muscle injury. We studied the completeness of the release of troponin T, a cardiac protein that is largely bound to myofibrillar structures and compared it with the release of cytoplasmic cardiac enzymes in 22 patients with AMI, who were treated with thrombolytic therapy.Creatine kinase (CK; EC 2.7.3.2), hydroxybutyrate dehydrogenase (HBDH), lactate dehydrogenase (LDH; EC 1.1.1.27) and troponin T were assayed serially in plasma samples obtained frequently and for at least 168 h after the start of thrombolytic therapy. Cumulative release of enzymes and troponin T in plasma were calculated by using a two-compartment model for circulating proteins.In order to express the cumulative plasma releases in gram equivalents (g-eq) healthy myocardium per litre plasma (infarct size), we determined HBDH, LDH and total troponin T contents per gram net weight of tissue in 17 human hearts obtained post-mortem from patients who died from non-cardiac causes. Mean (SD) tissue contents per gram wet weight of, respectively, l56±25 Ujg, 385±59 Ujg and 234 ± 65 Ji.gjg were found.For the cardiac enzymes CK, HBDH and LDH the mean (SEM, n = 22) total release over 72 h, was, respectively, 5·9 ± 1'5, 5·9 ± 1·6 and 6·1 ± 1·7 g-eqjL. There was no further increase after 72 h and the differences between enzymes were not significant. The mean (SEM) cumulative troponin T release, expressed in gram equivalents of myocardium per litre of plasma was only O· 30 ± 0·09 g-eqjL after 72 h and O' 51 ± 0·61 g-eq/L after 168 h. After 72 h total recovery of troponin T in g-eqjL was only 5% and after 168 h only 8·5% of the total recovery of cytoplasmic cardiac enzymes after 72 h.Cumulative troponin T release after 72 h and after 168 h correlates well with infarct size, estimated from cumulative cytoplasmic enzyme release. However, quantification of infarct size should preferably be performed from plasma release curves of cytoplasmic cardiac enzymes or proteins in order to prevent underestimation of infarct size, caused by incomplete release of the non-cytoplasmic proteins. Additional key phrases: compartmental model; reperfusion; intracellular compartmentation; quantification of tissue damage

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Section: Cardiac Troponin T Release 31s Patients and Memodsmentioning

confidence: 99%

Cardiac Troponin T Release into Plasma after Acute Myocardial Infarction: Only Fractional Recovery Compared with Enzymes

1996

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“…-stimulated ATPase and myosin ATPase activities were decreased in heart failure due to aging [22,123]. Both ATP consumption and Ca 2?…”

Section: Subcellular Defects In Aging Heartmentioning

confidence: 99%

“…-sensitivity of myofibrillar Mg 2? -ATPase in the aging myocardium [123]. In view of the increased oxidative stress, as a consequence of the generation of reactive oxygen and reactive nitrogen species in the aging heart, proteomic analysis has revealed an increase in the content of nitrated proteins including myosin heavy chain, neurofibromin, tropomyosin, and nebulin-related anchoring protein in cardiac muscle from the old animal [130].…”

Section: Subcellular Defects In Aging Heartmentioning

confidence: 99%

Cardiac remodeling and subcellular defects in heart failure due to myocardial infarction and aging

et al. 2011

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Although several risk factors including hypertension, cardiac hypertrophy, coronary artery disease, and diabetes are known to result in heart failure, elderly subjects are more susceptible to myocardial infarction and more likely to develop heart failure. This article is intended to discuss that cardiac dysfunction in hearts failing due to myocardial infarction and aging is associated with cardiac remodeling and defects in the subcellular organelles such as sarcolemma (SL), sarcoplasmic reticulum (SR), and myofibrils. Despite some differences in the pattern of heart failure due to myocardial infarction and aging with respect to their etiology and sequence of events, evidence has been presented to show that subcellular remodeling plays a critical role in the occurrence of intracellular Ca(2+)-overload and development of cardiac dysfunction in both types of failing heart. In particular, alterations in gene expression for SL and SR proteins induce Ca(2+)-handling abnormalities in cardiomyocytes, whereas those for myofibrillar proteins impair the interaction of Ca(2+) with myofibrils in hearts failing due to myocardial infarction and aging. In addition, different phosphorylation mechanisms, which regulate the activities of Ca(2+)-cycling proteins in SL and SR membranes as well as Ca(2+)-binding proteins in myofibrils, become defective in the failing heart. Accordingly, it is suggested that subcellular remodeling involving defects in Ca(2+)-handling and Ca(2+)-binding proteins as well as their regulatory mechanisms is intimately associated with cardiac remodeling and heart failure due to myocardial infarction and aging.

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Molecular and Cellular Phenotypes of Cardiovascular Aging

Marı́n-Garcı́a

Goldenthal

Moe

Aging and the Heart

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Proteolysis of myosin and troponin in human myocardium of elderly subjects.

Cited by 7 publications

References 29 publications

Cardiac Troponin T Release into Plasma after Acute Myocardial Infarction: Only Fractional Recovery Compared with Enzymes

Cardiac Troponin T Release into Plasma after Acute Myocardial Infarction: Only Fractional Recovery Compared with Enzymes

Cardiac remodeling and subcellular defects in heart failure due to myocardial infarction and aging

Molecular and Cellular Phenotypes of Cardiovascular Aging

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