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

MAPK activation and apoptotic alterations in hearts subjected to calcium paradox are attenuated by taurine.

OBJECTIVE: The Ca(2+)-paradox is an important phenomenon to study cell injury induced by Ca(2+)-overload in myocardium. Although intracellular Ca(2+)-overload acts as a trigger and modulator of cell death due to apoptosis under various pathophysiological conditions, the presence of apoptosis in hearts subjected to Ca(2+)-paradox has not been demonstrated. Since taurine attenuates the changes in cardiac function due to Ca(2+)-paradox, this study investigated the occurrence and mechanisms of apoptosis in Ca(2+)-paradoxic hearts treated in the absence and presence of taurine. METHODS: Ca(2+)-paradox was induced by perfusing the isolated rat heart with Ca(2+)-free medium for 5 min followed by reperfusion with Ca(2+)-containing medium for 30 min. Apoptosis related signal transduction mechanisms were determined in Ca(2+)-paradoxic hearts perfused with or without 10 mM taurine. RESULTS: Marked alterations in cardiac function and the presence of apoptosis were seen in Ca(2+)-paradoxic hearts reperfused for 30 min. Unlike the total protein contents in hearts subjected to Ca(2+)-paradox, the contents of phosphorylated p38 mitogen-activated protein kinase ( MAPK), extracellular signal regulated kinase (ERK)1, ERK2 and c-jun amino-terminal kinase were increased by 125+/-8.6%, 296+/-14.3%, 213+/-8.5% and 133+/-4.2%, respectively vs. control. Caspase-3 and phosphorylated Bcl-2 contents were also increased by 193+/-10.2% and 134+/-5.0% vs. control whereas phosphorylated Bad and the ratio of Bcl-2/Bad were depressed by 32+/-10.8% and 0.23+/-0.5% vs. control in Ca(2+)-paradoxic hearts. The apoptosis as seen in Ca(2+)-paradoxic hearts reperfused for 30 min was not evident in hearts at 10 min Ca(2+)-repletion but was similar to hearts subjected to 60 min Ca(2+)-repletion. These changes in the apoptotic pathway in cardiomyocytes subjected to Ca(2+)-paradox were prevented by taurine. Furthermore, taurine attenuated the KCl- or ATP-induced increase in intracellular concentration of Ca(2+) in cardiomyocytes. CONCLUSIONS: This study suggests that cardiac dysfunction due to Ca(2+)-paradox may be associated with apoptosis. In addition, the beneficial effects of taurine on cardiac function may be related to the attenuation of changes in MAPK and apoptotic signal transduction mechanisms in Ca(2+)-paradoxic hearts.[1]

References

  1. MAPK activation and apoptotic alterations in hearts subjected to calcium paradox are attenuated by taurine. Xu, Y.J., Saini, H.K., Zhang, M., Elimban, V., Dhalla, N.S. Cardiovasc. Res. (2006) [Pubmed]
 
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