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. Author manuscript; available in PMC: 2015 Oct 1.
Published in final edited form as: Exp Eye Res. 2014 Jun 18;127:20–25. doi: 10.1016/j.exer.2014.06.002

Figure 2.

Figure 2

(A) By real time PCR, Cox2, Chop, and Grp78 mRNAs were overexpressed (*p<0.05) in the endothelium of mutant mice untreated with NAC (L450W-Control) compared to wild-type mice untreated with NAC (WT-Control, relative quantity (RQ) = 1), indicating increased oxidative and ER stress in mutant endothelium. (B) By real time PCR, iNos mRNA was overexpressed, but Chop and Grp78 mRNAs were underexpressed (*p<0.05) in mutant mice treated with NAC (L450W-NAC) compared to mutant mice untreated with NAC (L450W-Control, RQ=1), indicating increased antioxidant defense and decreased ER stress in L450W mutant endothelium associated with NAC treatment. Western blotting (C) with densitometry normalized to β-actin (ActB) (D) shows increased levels of iNos, but decreased levels of Grp78 and Chop (*p<0.05), in mutant mice treated with NAC (L450W-NAC) compared to mutant mice untreated with NAC (L450W-Control), indicating increased antioxidant defense and decreased ER stress in L450W mutant endothelium associated with NAC treatment.