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Published in final edited form as: Glia. 2010 Dec 29;59(3):486–498. doi: 10.1002/glia.21118

Glioma-conditioned medium (GCM) and S100B suppressed microglia (MG) and bone marrow-derived monocytes (BMM). N9 MG or BMM (0.2 × 10⁶ cells/well) were incubated in regular medium (control), GCM, or different doses of S100B for 6–48 h. (A) Western blots demonstrating inhibition of p38 and p42 by GCM and low levels of S100B. (B) FACS analysis demonstrating inhibition of TNF-α expression by N9 cells after a 24-h incubation with GCM or S100B. (C) RT-PCR demonstrating inhibition of IL-1β expression by GCM and low levels of S100B at baseline (left) and following stimulation with LPS for 12 h (right). (D) GCM and low-dose S100B (50 nM) inhibited IL-1β expression by BMM. IL-1β inhibition was partially reversed when S100B was depleted from GCM (DCM) by S100B Abs but not control IgG. Experimental results are representative of at least two separate experiments. (n=3 to 4 samples/group, ±SEM)

Glioma-conditioned medium (GCM) and S100B suppressed microglia (MG) and bone marrow-derived monocytes (BMM). N9 MG or BMM (0.2 × 10⁶ cells/well) were incubated in regular medium (control), GCM, or different doses of S100B for 6–48 h. (A) Western blots demonstrating inhibition of p38 and p42 by GCM and low levels of S100B. (B) FACS analysis demonstrating inhibition of TNF-α expression by N9 cells after a 24-h incubation with GCM or S100B. (C) RT-PCR demonstrating inhibition of IL-1β expression by GCM and low levels of S100B at baseline (left) and following stimulation with LPS for 12 h (right). (D) GCM and low-dose S100B (50 nM) inhibited IL-1β expression by BMM. IL-1β inhibition was partially reversed when S100B was depleted from GCM (DCM) by S100B Abs but not control IgG. Experimental results are representative of at least two separate experiments. (n=3 to 4 samples/group, ±SEM)