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. Author manuscript; available in PMC: 2011 Feb 5.
Published in final edited form as: Circ Res. 2009 Dec 3;106(2):354. doi: 10.1161/CIRCRESAHA.109.207423

Figure 8. Involvement of mitochondrial Ca2+ in myocyte death in PLN-KO/CaMKII-TG mice.

Figure 8

A, Mitochondrial Ca2+ was measured as shown in the protocol. NT: no treatment; Thaps: thapsigargin. B, Mitochondrial Ca2+ was increased in cardiomyocytes isolated from PLN-KO/CaMKII-TG mice. *P<0.05 vs. WT. Mitochondrial Ca2+ in PLN-KO/CaMKII-TG myocytes returned to control levels with reduced external Ca2+ (0.3 mM) and CaMKII inhibitor AIP. C, Reduced external Ca2+ and CaMKII inhibition with AIP returned SR Ca2+ content and Ca2+ transients to near control myocyte levels. D, Inhibition of the mitochondrial uniporter by Ru-360 or inhibition of the mitochondrial permeability transition pore by cyclosporine A decreased the rate of death in isolated cardiomyocytes from PLN-KO/CaMKII-TG mice at 12 hours. *P<0.05 vs. WT.