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. Author manuscript; available in PMC: 2010 Apr 24.
Published in final edited form as: Circ Res. 2009 Mar 19;104(8):1012–1020. doi: 10.1161/CIRCRESAHA.108.189811

Figure 8.

Figure 8

I-1c attenuates the I/R-induced ER stress response. A, Immunoblot analysis of protein disulphide isomerase (PDI) and Grp78 revealed that the ER stress response was induced in WT hearts, whereas it was unaltered in DTG hearts on I/R ex vivo. B, Quantitative analysis of the blots in A, normalized to actin. C, Inositol-requiring enzyme 1α (Ire1α) increased in WT hearts post-I/R but remained unaltered in DTG hearts. D, Caspase-12 activity was increased post-I/R in WT hearts, but it was reduced to preischemic values in DTG hearts. Bars represent means±SEM (WT, n=4; DTG, n=4). *P<0.05 vs WT I/R, #P<0.05 vs preischemic values in each group. E, DNA fragmentation was attenuated in Ad.I-1c–infected myocytes after sI/R (1 hour of ischemia/3 hours of reperfusion). F, ER stress induction was attenuated in Ad.I-1c–infected myocytes. Bars represent means±SEM (WT, n=4; DTG, n=4). *P<0.05 vs Ad.GFP basal.