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. 2012 Mar 14;18(1):785–793. doi: 10.2119/molmed.2011.00466

Figure 4.

Figure 4

Effect of ALDH2 overexpression on ER stress in cardiomyocytes. (A) ALDH2 expression was increased by ALDH2 adenoviral vector. Increased expression of GRP78 (B), p-eIF2 (C) and CHOP (D) were abrogated by ALDH2 overexpression. Effect of ALDH2 vector on ER stress was not affected by LY294002. (E) p47phox subunit upregulation by tunicamycin (TN) was mitigated by the ALDH2 vector compared with TN treatment group, effect of which was blocked by LY294002. (F) Depressed p-Akt by TN was activated by ALDH2 vector compared with the TN treatment group. ALDH2 vector and LY294002 alone did not increase ER stress markers and p47phox subunit. Ad-ALDH2, ALDH2 adenoviral vector. All values for given protein expression were normalized to that of GAPDH. The data (presented as percentages of control) are means ± SEM of three separate experiments. *p < 0.05 versus control; #p < 0.05 versus TN group; †p < 0.05 versus Ad-ALDH2 + TN group.