Enhancement of Cellular Antioxidant-Defence Preserves Diastolic Dysfunction via Regulation of Both Diastolic Zn2+ and Ca2+ and Prevention of RyR2-Leak in Hyperglycemic Cardiomyocytes
Figure 7
Direct effects of external Zn2+ on RyR2 macromolecular complex of ventricular heart tissue. (a) Top: representative Western blot images for phospho-RyR2-Ser2808 (pRyR2), FK-binding protein, calstabin2 (FKBP), protein kinase A (PKA), phosphorylated PKA (phospho-PKA-Thr198), Ca2+-calmodulin-dependent kinase (CaMKII), phosphorylated CaMKII (phospho-CaMKII-Thr286), nuclear factor kappaB (NF-κB), phosphorylated NF-κB (phosoho-NF-κB), β-actin. (b) Quantification for the ratio of pRyR2 to RyR2, FKBP to β-actin, pPKA to PKA, pCaMKII to CaMKII and pNF-κB to NF-κB. Data presented in (b) obtained from control (CON), 1 μM ZnCl2 incubated control (+ZnCl2, light gray), diabetic (DM) and 1 μM ZnCl2 incubated diabetic (+ZnCl2, dark gray) rat heart homogenates. Bar graphs represent mean ± SEM ( for each protocol/group). Significant at * versus CON and † versus DM.
