Fig. 4.
Roles of CaMKII and PKC signaling on KATP channel trafficking during ischemia and IPC. Mouse hearts were perfused with the CaMKII inhibitor (KN-93, or KN; 0.5 μM) or the PKC inhibitor chelerythrine (3 μM) before subjecting the hearts to ischemia or IPC protocols (or a no-ischemia control). A: sarcolemmal (SL) and endosomal (E) membrane preparations were subjected to immunoblotting with an anti-Kir6.2 antibody. B: fractions of SL Kir6.2 in the presence of KN-93: control (n = 3), ischemia (n = 3), and IPC (n = 3). Fractions of SL Kir6.2 in the presence of chelerythrine are also shown: control (n = 4), ischemia (n = 4), and IPC (n = 4). *P < 0.05 vs. the control group.