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Mol Cell Biochem. 2004 Aug;263(1):91-7. doi: 10.1023/B:MCBI.0000041851.53074.72.

The slow skeletal muscle troponin T gene is expressed in developing and diseased human heart.

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National Heart and Lung Institute, Imperial College, London, Heart Science Centre, Harefield, Middlesex, UB9 6JH, UK.
Department of Basic Sciences, Royal Veterinary College, Royal College Street, London, NW1 0TU, UK.


Cardiac muscle development is characterised by the activation of contractile protein genes and subsequent modulation of expression resulting, ultimately, in the formation of a mature four-chambered organ. Myocardial gene expression is also altered in the adult in response to pathological stimuli and this is thought to contribute to the altered contractile characteristics of the diseased heart. We have examined the expression of the slow skeletal troponin T (TnT) gene in the human heart during development and in disease using whole mount in situ hybridisation and real-time quantitative (TaqMan) polymerase chain reaction (PCR). Slow skeletal TnT mRNA shows transitory and regional expression in the early foetal heart, which occurs at different times in atria and ventricles. In ventricular myocardium, expression is seen in the outer epicardial layer at a time when the coronary circulation is being established. Expression was detected at low levels in the adult human heart and was significantly increased in end-stage heart failure. Similarly, expression was readily detectable during early rat heart development and was up-regulated in pressure overload hypertrophy in adult. Together these data show for the first time that slow skeletal TnT mRNA is readily detectable during early human heart development. They further suggest that slow skeletal TnT may be responsive to myocardial stress and that elevated levels may contribute to myocardial dysfunction in adult disease. (Mol Cell Biochem 263: 91-97, 2004).


development; end-stage heart failure; hypertrophy; troponin T

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