FIGURE 4.

HDAC8 modulates gene expression in GAMs. (a) rtPCR of anti‐ (arg‐1, chil3, tgfβ and retnla) and pro‐inflammatory (tnfα, il1β, nos2, and cd86) genes in CD11b⁺ cells sorted from ipsi‐ and contralateral hemisphere of CT2A‐bearing mice treated with vehicle or PCI‐34051 40 mg/kg, as indicated. Data are the mean ± S.E.M. versus vehicle contra (n = 6 mice per condition, *P < 0.05 **P < 0.05, one‐way ANOVA). (b) rtPCR analysis of anti‐ (arg‐1, chil3, tgfβ and retnla) and pro‐inflammatory (tnfα, il1β, nos2 and cd86) genes in primary microglia incubated with vehicle, IL‐4 or LPS + IFN‐γ for 48 h, in presence or not of PCI‐34051 10 μM. Data are the mean ± S.E.M. expressed as fold increased in comparison with vehicle‐treated microglia (n = 5, **P < 0.01, one‐way ANOVA). (c) rtPCR of human pro‐ (cxcl10, nos2, and il12a) and anti‐inflammatory (cd163, mmp12 and tgfβ) genes in CD11b⁺ cells sorted from patient‐derived GBM tissue, after tissue treatment with PCI‐34051(10 μM, 48 h) or vehicle. Above: Scheme of human GBM treatment. Data are the mean ± S.E.M., n = 5, *P < 0.05 versus vehicle, Student's t‐test