Fig. 3. Protein kinase C δ (PKCδ ) colocalization with subcellular targets in response to ischemic preconditioning (IPC ) and anesthetic preconditioning (APC ). (A  and B ) There was clear translocation of PKCδ (red ) to mitochondria (green ) in IPC and APC (colocalization indicated in yellow ), which was inhibited by chelerythrine (CHE ) (IPC, 10 μm; APC, 5 μm) and rottlerin (ROT) (IPC, 0.2 μm; APC, 0.1 μm). (C ) No translocation of PKCδ (red ) to the sarcolemma (green ) was observed in both types of preconditioning. Note that there was no translocation of PKCδ to mitochondria and sarcolemma in control hearts (CTLLD= hearts with time-matched perfusion on the Langendorff apparatus). Pictures represent epifluorescence micrographs with ×400 magnification. *Significantly increased compared with CTLLD, P < 0.05. †Not significantly different from CTLLD.

Fig. 3. Protein kinase C δ (PKCδ ) colocalization with subcellular targets in response to ischemic preconditioning (IPC ) and anesthetic preconditioning (APC ). (A  and B ) There was clear translocation of PKCδ (red ) to mitochondria (green ) in IPC and APC (colocalization indicated in yellow ), which was inhibited by chelerythrine (CHE ) (IPC, 10 μm; APC, 5 μm) and rottlerin (ROT) (IPC, 0.2 μm; APC, 0.1 μm). (C ) No translocation of PKCδ (red ) to the sarcolemma (green ) was observed in both types of preconditioning. Note that there was no translocation of PKCδ to mitochondria and sarcolemma in control hearts (CTLLD= hearts with time-matched perfusion on the Langendorff apparatus). Pictures represent epifluorescence micrographs with ×400 magnification. *Significantly increased compared with CTLLD, P < 0.05. †Not significantly different from CTLLD.

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