Cardiac Troponin T Isoform Expression Correlates With Pathophysiological Descriptors in Patients Who Underwent Corrective Surgery for Congenital Heart Disease

Saba, Ziad; Nassar, Rashid; Ungerleider, Ross M.; Oakeley, A. E.; Anderson, Page A.W.

doi:10.1161/01.cir.94.3.472

Cited by 46 publications

(28 citation statements)

References 19 publications

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“…And they claimed cTnT4 might not be responsible for myocardial failure but might be a consequence of hemodynamic stress. Their finding is in agreement with the previous reports (Saba et al 1996;Mesnard-Rouiller et al 1997) that cTnT4 protein increased in only half the failing hearts, and correlated with the duration of inotropic support, suggesting its increase might not be associated with heart failure but might be related to hemodynamic stress. This suggestion might be consistent with our finding, i.e., the predisposition to cardiac hypertrophy.…”

Section: Discussionsupporting

confidence: 93%

The role of a common TNNT2 polymorphism in cardiac hypertrophy

et al. 2004

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We found a five-basepair insertion/deletion polymorphism in intron 3 of TNNT2, one of the genes responsible for hypertrophic cardiomyopathy. These five bases may be part of an intronic polypyrimidine tract sequence that may affect splicing. The purpose of the study was to examine the association of the polymorphism with cardiac hypertrophy. The study population consisted of 151 subjects with prominent concentric left ventricular hypertrophy, and 987 healthy subjects recruited from medical checkups (control population). The deletion/deletion genotype tended to be associated with a larger left ventricular mass/height ratio in the HCM population (p<0.0001). Multiple regression analyses indicated that the left ventricular mass/height ratio was determined (p<0.0001, R=0.738) by the TNNT2geno-type. Moreover, the frequency of the deletion allele was significantly higher in the hypertrophy population than in the control population (p<0.0001). In vitro expression study revealed the deletion allele significantly affected the mRNA expression pattern by skipping exon 4 during splicing. In conclusion, TNNT2 deletion allele could be associated with a predisposition to prominent left ventricular hypertrophy.

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Section: Discussionsupporting

confidence: 93%

The role of a common TNNT2 polymorphism in cardiac hypertrophy

et al. 2004

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“…Troponin C functions as a calciumreceptor while troponin I prevents the adenosine triphosphatase activity when bound to actin. Troponin T fixes the troponin group to tropomyosin 29) . After myocardial cell damage, troponins are released from the myocytes.…”

Section: Discussionmentioning

confidence: 99%

Initial Troponin Level as a Predictor of Prognosis in Patients with Intracerebral Hemorrhage

Chung

Won

Kwon

et al. 2009

J Korean Neurosurg Soc

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Objective : It has been suggested that elevated cardiac troponin T (cTnT) level is a marker of increased risk of mortality in acute ischemic stroke and subarachnoid hemorrhage (SAH). However, the association of serum cTnT level and prognosis of intracerebral hemorrhage (ICH) has been sparsely investigated. The aim of this study was to identify the relationship between cTnT level and the outcome in patients with spontaneous ICH. Methods : We retrospectively investigated 253 patients identified by a database search from records of patients admitted in our department for ICH between January 1, 2003 and December 31, 2007. The patients were divided into 2 groups; the patients in group 1 (n=225) with serum cTnT values of 0.01 ng/mL or less, and those in group 2 (n=28) with serum cTnT values greater than 0.01 ng/mL. Results : The serum cTnT level was elevated in 28 patients. There were significant differences in sex, hypertension, creatine kinase-myocardial band, midline shift, side of hematoma, and presence of intraventricular hemorrhage between the 2 groups. Logistic regression analysis identified the level of consciousness on admission, cTnT and midline shift as independent predictors of hospital mortality. Conclusion : Theses results suggest that increased serum cTnT level at admission is associated with in-hospital mortality and the addition of a serum cTnT assay to routine admission testing should be considered in patients with ICH.

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Section: Marston and Redwood Thin Filament Isoform Switching And Protmentioning

confidence: 99%

“…All of these studies reported decreased maximally activated myofibrillar ATPase activity, unloaded shortening or sliding speed, and increased Ca 2ϩ sensitivity in failing heart muscle independently of whether the putative T4 band was present in the sample. 53,54,[57][58][59] It is possible that a particular subset of patients with heart failure reexpress TnT4 isoform; however, the possibility that the higher mobility band, when observed, could be a proteolytic fragment of TnT3 was suggested by the work of Knott and colleagues 56,58 and has not been ruled out in other studies.The physiological significance of fetal troponin T isoform reexpression in failing heart now seems doubtful. At most, 10% to 20% of cardiac troponin T is altered in vivo in some failing hearts, and recent studies indicate that the functional differences between TnT3 and TnT4 are minimal and could not solely account for the observed increased Ca 2ϩ sensitivity found in failing heart muscle.…”

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confidence: 99%

Modulation of Thin Filament Activation by Breakdown or Isoform Switching of Thin Filament Proteins

Marston

Redwood

2003

Circulation Research

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Abstract-In the heart, the contractile apparatus is adapted to the specific demands of the organ for continuous rhythmic contraction. The specialized contractile properties of heart muscle are attributable to the expression of cardiac-specific isoforms of contractile proteins. This review describes the isoforms of the thin filament proteins actin and tropomyosin and the three troponin subunits found in human heart muscle, how the isoform profiles of these proteins change during development and disease, and the possible functional consequences of these changes. During development of the heart, there is a distinctive switch of isoform expression at or shortly after birth; however, during adult life, thin filament protein isoform composition seems to be stable despite protein turnover rates of 3 to 10 days. The pattern of isoforms of actin, tropomyosin, troponin I, troponin C, and troponin T is not affected by aging or heart disease (ischemia and dilated cardiomyopathy). The evidence for proteolysis of thin filament proteins in situ during ischemia and stunning is evaluated, and it is concluded that C-terminal cleavage of troponin I is a feature of irreversibly injured myocardium but may not play a role in reversible stunning. Key Words: actin Ⅲ troponin Ⅲ tropomyosin Ⅲ calpain Ⅲ stunning T he contractile apparatus of muscle is made up from interdigitating thick and thin filaments arrayed in sarcomeres. Contraction is attributable to the sliding of thick filaments past thin filaments and is powered by the molecular motor of the myosin crossbridge cyclically attaching to actin, changing conformation, and detaching. Contractility is controlled by sarcoplasmic Ca 2ϩ , which acts on the receptor molecules troponin and tropomyosin in the thin filaments. 1 Native thin filaments are built up from a double helix of actin monomers, with the elongated tropomyosin molecule forming a continuous strand along each actin helix and the troponin complex bound every 7th actin. Troponin is made up from three subunits. Troponin I is the inhibitory protein that binds to actin and prevents myosin crossbridge cycling. Troponin C is the Ca 2ϩ -binding component; at micromolar Ca 2ϩ concentrations, Ca 2ϩ is bound to troponin C which then binds to troponin I, releasing it from its inhibitory site on actin. Troponin T is an elongated molecule that binds to both troponin C and troponin I and also to tropomyosin, thus anchoring the complex on the thin filament. The interaction Original received September 17, 2003; revision received October 20, 2003; accepted October 23, 2003. From the Imperial College London (S.B.M.), National Heart and Lung Institute, London, UK, and Department of Cardiovascular Medicine (C.S.R.), University of Oxford, UK.Correspondence to Steven B. Marston, Imperial College London, National Heart and Lung Institute, Dovehouse St, London SW3 6LY, UK. E-mail S. Marston@imperial.ac.uk © 2003 American Heart Association, Inc. of the troponin complex with tropomyosin propagates the regulatory signal from 1 troponin to up to 14 a...

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Cardiac Troponin T Isoform Expression Correlates With Pathophysiological Descriptors in Patients Who Underwent Corrective Surgery for Congenital Heart Disease

Abstract: These findings suggest that in patients with congenital cardiac defects, cTnT4 expression is modulated by heart failure and is increased in hearts that are more hemodynamically stressed.

Cited by 46 publications

References 19 publications

The role of a common TNNT2 polymorphism in cardiac hypertrophy

The role of a common TNNT2 polymorphism in cardiac hypertrophy

Initial Troponin Level as a Predictor of Prognosis in Patients with Intracerebral Hemorrhage

Modulation of Thin Filament Activation by Breakdown or Isoform Switching of Thin Filament Proteins

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