Ca⁺²/Calmodulin-Dependent Protein Kinase Mediates Glucose Toxicity-Induced Cardiomyocyte Contractile Dysfunction

Figure 5

Expression of intracellular Ca²⁺ regulatory proteins in rat cardiomyocytes cultured for 12 hours in a serum-free medium with normal glucose (NG: 5.5 mM) or high glucose (HG: 25.5 mM) in the absence or presence of high extracellular Ca²⁺ (Hi-Ca, 2.7 mM) in the recording contractile buffer. An extracellular Ca²⁺ concentration of 1.0 mM was used as the normal low Ca²⁺ (LoCa) environment. (a) Representative gel blots depicting levels of SERCA2a, Na⁺-Ca²⁺ exchanger, phospholamban, and GAPDH (loading control), (b) SERCA2a expression, (c) Na⁺-Ca²⁺ exchanger expression, (d) phospholamban expression, and (e) SERCA activity measured using ⁴⁵Ca²⁺ uptake. Mean ± SEM, 𝑛=6-7 isolations per group, *𝑃<0.05 versus NG-LoCa group, ^#𝑃<0.05 versus HG-LoCa group.

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