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. Author manuscript; available in PMC: 2015 May 4.
Published in final edited form as: Biochim Biophys Acta. 2015 Feb 4;1852(5):882–892. doi: 10.1016/j.bbadis.2015.01.019

Fig. 5.

Fig. 5

(A–D) Role of calpain in ER stress and JNK1/2 activation following H/R. H9c2 cells were infected with Ad-CAST or Ad-gal, and then subjected to a 24-hour hypoxia followed by a 24-hour re-oxygenation. (A) Representative western blots from 3 different experiments for GRP78, CHOP, pPERK and GAPDH. (B) Representative western blots from 3 different experiments for phosphorylated JNK1/2 and JNK1/2. (C and D) Quantification for the ratio of phosphorylated JNK1/2 over JNK1/2. Data are mean ± SD from 3 different experiments. *P < 0.05 vs Ad-gal + Sham and #P < 0.05 vs Ad-gal + H/R. (E–H) Effects of calpain-1 knockdown on ER stress and apoptosis in H9c2 cells following H/R. H9c2 cells were transfected with siRNA for calpain-1 or control siRNA. Twenty-four hours after transfection, the cells were subjected to H/R. (E) Representative western blot for capn1 and GAPDH proteins from 3 different cultures. (F) Representative western blots for ER stress markers (GRP78, phosphorylated PERK (pPERK), CHOP, phosphorylated JNK1/2, and JNK1/2) from 3 different cultures show that silencing calpain-1 reduces H/R-induced ER stress. (G) Caspase-3 activity and (H) DNA fragmentation. Data are mean ± SD from 3 different experiments. *P < 0.05 vs Sham + Control siRNA and #P < 0.05 vs H/R + Control siRNA.