Figure 3
Figure 3. Egr-1 expression is up-regulated in HBMECs exposed to cocaine. (A) Cocaine induced time-dependent activation of Egr-1 expression in HBMECs. (B) Pharmacologic inhibition of ERK and JNK pathways by MEK (U0126) and JNK (SP600125) inhibitors resulted in amelioration of cocaine-mediated induction of Egr-1. (C) Transfection of cells with DN-MEK but not WT-MEK resulted in abrogation of cocaine-mediated induction of Egr-1. (D) Pretreatment of cells with MEK (U1026) and JNK (SP600125) but not PI3K (LY294002) inhibitors resulted in amelioration of cocaine-mediated induction of PDGF-BB. All data are presented as mean ± SD of 3 individual experiments. *P < .05, **P < .01 vs control group; #P < .05, ##P < .01 vs cocaine-treated group.

Egr-1 expression is up-regulated in HBMECs exposed to cocaine. (A) Cocaine induced time-dependent activation of Egr-1 expression in HBMECs. (B) Pharmacologic inhibition of ERK and JNK pathways by MEK (U0126) and JNK (SP600125) inhibitors resulted in amelioration of cocaine-mediated induction of Egr-1. (C) Transfection of cells with DN-MEK but not WT-MEK resulted in abrogation of cocaine-mediated induction of Egr-1. (D) Pretreatment of cells with MEK (U1026) and JNK (SP600125) but not PI3K (LY294002) inhibitors resulted in amelioration of cocaine-mediated induction of PDGF-BB. All data are presented as mean ± SD of 3 individual experiments. *P < .05, **P < .01 vs control group; #P < .05, ##P < .01 vs cocaine-treated group.

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