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

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Ho, Y.L. et al.

The correlation between expression of apoptosis-related proteins and myocardial functional reserve evaluated by dobutamine stress echocardiography in patients with dilated cardiomyopathy.

The relation between myocardial functional changes and the apoptosis-related proteins in patients with dilated cardiomyopathy (DCM) has not yet been reported. The purpose of this study was to assess this issue through the use of dobutamine stress echocardiography. A total of 81 segments of left ventricles (from 6 patients with DCM) were collected in this study. Segments from another 5 patients who had died of noncardiac causes were used as the control. Apoptosis-related proteins (bax, bcl-2, and p53) and apoptosis were evaluated in these segments by immunocytochemical stain and terminal deoxynucleotidyl transferase-mediated DNA nick end-labeling assay. There were 26 segments with dobutamine-induced contractile reserve. There were significant differences in numbers of segments with overexpression of bcl-2 and bax in the study and control groups. However, p53 was not found in either group. The total terminal deoxynucleotidyl transferase-mediated DNA nick end-labeling-positive nuclei in explanted hearts of DCM was 0.73%. The myocardial contractile reserve was inversely associated with an overexpression of bcl-2 (P <.01) rather than bax. In conclusion, the expression of bax and bcl-2 proteins in patients with DCM is enhanced and independent of p53. Loss of contractile reserve is associated with overexpression of bcl-2 protein in failing myocardium.[1]

References

The correlation between expression of apoptosis-related proteins and myocardial functional reserve evaluated by dobutamine stress echocardiography in patients with dilated cardiomyopathy. Ho, Y.L., Chen, C.L., Hsu, R.B., Lin, L.C., Huang, P.J. Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography. (2003) [Pubmed]

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