Inhibition of JNK Aggravates the Recovery of Rat Hearts after Global Ischemia: The Role of Mitochondrial JNK
Figure 6
Co-immunoprecipitation of mitochondrial proteins with P-JNK and P-p38.
Representative immunoblots showing interaction between P-JNK, P-p38, the MPTP components ANT, VDAC, CyP-D, and components of mitochondrial oxidative phosphorylation. (A) Cardiac mitochondria from each group were immunoprecipitated (IP) with P-JNK and P-p38. The complexes were subjected to SDS-PAGE followed by immunoblotting (IB) with indicated antibodies. Bands that underwent densitometry analysis are indicated by arrows (a,b). (B) Densitometric data for UQCRC2 (a component of mitochondrial complex III), were normalized to P-JNK. CS, non-ischemic hearts perfused for 60 min with 10 µM SU3327 added at 20 min after beginning of perfusion (n = 4). *, #, &: significantly different from the other indicators (P<0.05). (C) Densitometric data for UQCRC2 (a component of mitochondrial complex III), normalized to P-p38. n = 3 per group.