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. Author manuscript; available in PMC: 2015 Feb 1.
Published in final edited form as: Transl Stroke Res. 2013 Nov 27;5(1):118–127. doi: 10.1007/s12975-013-0312-z

Figure 2. The effect of EPO treatment on ROS formation, HIF-1α and PHD-2 expression in the presence of EPO and PHD-2 inhibition.

Figure 2

(A) HIF-1α protein expression in the presence and absence of EPOR chimera a competitive inhibitor of EPO. (B) Densiometric quantification of PHD-2 expression in the presence or absence of EPOR chimera (C) ROS formation during OGD in the presence or absence of EPO inhibitor. (D) HIF-1α expression after OGD in the presence of PHD-2 siRNA. (E) PHD-2 expression after OGD in the presence of siRNAs. (F) ROS formation during OGD in the presence or absence of PHD-2 siRNA. Data represent the mean and (± SD) n=6 in all groups. *P<0.01 compared to normoxia. #P< 0.01 compared to 10U/ml EPO treated group. &P<0.05 compared to Normoxia+Control siRNA. δP< 0.01 compared to PHD-2siRNA +EPO. One-way ANOVA was used for all analysis. pH P=0.015 using Kruskal-Wallis ANOVA on Ranks. HIF-1α P ≤ 0.001, using Kruskal-Wallis ANOVA on Ranks. PHD-2 P < 0.001. Inhibition of EPO or PHD-2 enhanced HIF-1α expression and ROS formation.