Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Schultz, J.e.l. .J. et al.

Accelerated onset of heart failure in mice during pressure overload with chronically decreased SERCA2 calcium pump activity.

We recently developed a mouse model with a single functional allele of Serca2 (Serca2+/-) that shows impaired cardiac contractility and relaxation without overt heart disease. The goal of this study was to test the hypothesis that chronic reduction in sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA)2 levels in combination with an increased hemodynamic load will result in an accelerated pathway to heart failure. Age-matched wild-type and Serca2+/- mice were subjected to 10 wk of pressure overload via transverse aortic coarctation surgery. Cardiac hypertrophy and heart failure were assessed by echocardiography, gravimetry/histology, hemodynamics, and Western blotting analyses. Our results showed that approximately 64% of coarcted Serca2+/- mice were in heart failure compared with 0% of coarcted wild-type mice (P < 0.05). Overall, morbidity and mortality were greatly increased in Serca2+/- mice under pressure overload. Echocardiography assessment revealed a significant increase in left ventricular (LV) mass, and LV hypertrophy in coarcted Serca2+/- mice converted from a concentric to an eccentric pattern, similar to that seen in human heart failure. Coarcted Serca2+/- mice had decreased contractile/systolic and relaxation/diastolic performance and/or function compared with coarcted wild-type mice (P < 0.05), despite a similar duration and degree of pressure overload. SERCA2a protein levels were significantly reduced (>50%) in coarcted Serca2+/- mice compared with noncoarcted and coarcted wild-type mice. Our findings suggest that reduction in SERCA2 levels in combination with an increased hemodynamic load results in an accelerated pathway to heart failure.[1]

References

Accelerated onset of heart failure in mice during pressure overload with chronically decreased SERCA2 calcium pump activity. Schultz, J.e.l. .J., Glascock, B.J., Witt, S.A., Nieman, M.L., Nattamai, K.J., Liu, L.H., Lorenz, J.N., Shull, G.E., Kimball, T.R., Periasamy, M. Am. J. Physiol. Heart Circ. Physiol. (2004) [Pubmed]

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