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. Author manuscript; available in PMC: 2012 Jan 1.
Published in final edited form as: Glia. 2010 Sep 27;59(1):1–13. doi: 10.1002/glia.21071

Figure 6. BzATP-induced alterations in LPS-stimulated NO and TNF-α production requires the P2X7-Egr pathway.

Figure 6

Parental N9, shP2X7/N9 and shEgr/N9 cells were treated with vehicle (250 mM Hepes), LPS (1 μg/mL), or LPS+BzATP (150 μM) overnight. (A) BzATP-mediated inhibition of LPS-stimulated iNOS expression does not occur in shP2X7/N9 and shEgr/N9 cells. (B) BzATP-mediated augmentation of LPS-induced TNF-α expression is abrogated in shP2X7/N9 and shEgr/N9 cells. (C) Expression of TGF-β and β-actin are unchanged in shEgr/N9 cells treated with vehicle or LPS. (D) BzATP treatment increases LPS-stimulated IL-10 mRNA levels in both parental N9 and shEgr/N9 cells. The means ± SEM are graphed as fold induction relative to vehicle treatment (C) or LPS treatment (A, B, D) in 3-8 independent experiments. * p<0.05, **p<0.01, ***p<0.001 vs. vehicle or LPS treatment.