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Figure 3 | Cardiovascular Diabetology

Figure 3

From: Protection of the heart by treatment with a divalent-copper-selective chelator reveals a novel mechanism underlying cardiomyopathy in diabetic rats

Figure 3

Alterations in SERCA2a and NCX in LV myocardium. (A) Caffeine-induced Ca2+ transients were recorded from cardiomyocytes isolated from each group of rats, which were exposed to a series of solution changes as described in methods. (i) shows examples of normalized caffeine-induced Ca2+ transients from a single cell, with pooled data shown in (ii)&(iii). There was no significant difference in the time-constant of decay of caffeine-induced Ca2+ transients among groups in either of the caffeine perfusion solutions, indicating no change of NCX activity among groups. These data suggest that the slower decay of the Ca2+ transient in diabetic rats did not arise from differences in NCX function. Consistently, a western blotting study (B) showed no significant change in NCX levels (molecular weight 120 kDa, n = 8 in each group) among groups, but decreased expression of SERCA2a (molecular weight 110 kDa, n = 7 in each group) in diabetic rats. TETA had no effect on levels of either transporter. C: Control (Open bars); D: Diabetic (Solid bars); D + T: TETA-treated diabetic (Patterned bars). Data are means ± SEM, one-way Kruskal-Wallis ANOVA with post-hoc application of Dunn’s Multiple Comparisons test (P = 0.0007): * C vs D, P < 0.05; † C vs D + T, P < 0.05.

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