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. Author manuscript; available in PMC: 2008 Oct 1.
Published in final edited form as: J Mol Cell Cardiol. 2007 Aug 8;43(4):420–428. doi: 10.1016/j.yjmcc.2007.07.061

Fig 4. δPKC modulates the ER stress response of the myocardium in a model of cardiac ischemia and reperfusion injury.

Fig 4

A. Normoxic control hearts and hearts that underwent ischemia and reperfusion were homogenized and total extracts were isolated. The levels of GRP78, spliced XBP1 and phospho-JNK were determined by Western blot.

B. Quantitative data of the hearts described in (A). Values represent mean ± S.E. of three animals in each group (N: normoxia; I/R: ischemia/reperfusion). Student t test; * p<0.05 vs. TAT treatment, # p< 0.05 vs. control.

C. Hearts were subjected to ischemia-reperfusion and treated at the onset of reperfusion with TAT control peptide or δV1-1 and the infarct size (left panel) and cell survival, as demonstrated by the decrease in CPK release (right panel), were determined. Data are expressed as mean ± S.E. of three animals in each group. Student t test; * p<0.05 vs. TAT treatment.