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. Author manuscript; available in PMC: 2015 Jan 21.
Published in final edited form as: J Neurosci Res. 2010 Nov 1;88(14):3090–3101. doi: 10.1002/jnr.22458

Fig. 1.

Fig. 1

PI3K inhibitor and CCR5 antibodies diminished HIV-1-induced activation of STAT1 and STAT3. Exposure of HBMEC to infectious viral particles induced the phosphorylation of STAT1 (A,C,D) and STAT3 (B,E) at serine-727. PI3K inhibitors diminished HIV-1 induced activation and expression of STAT1 (A) and STAT3 (B) in a dose-dependent manner, with maximal inhibition at 50 μM. CCR5 antibodies (20 μg/ml) significantly diminished virus-induced phosphorylation of STAT1 (C) and STAT3 (E), whereas isotype-matched antibody control had no effect (D). ★★P < 0.01, ★★★P < 0.001. Representative data from three independent experiments. Primary HBMEC from different human donors were used for these experiments, and the minor differences observed in basal levels of phosphorylated STAT are due to interdonor variability.