MSX3 Switches Microglia Polarization and Protects from Inflammation-Induced Demyelination

(Downloading may take up to 30 seconds. If the slide opens in your browser, select File -> Save As to save it.)

Click on image to view larger version.

Figure 9.
Figure 9.

MSX3 promotes PPARγ, STAT6, and JAK3 expression in microglia. A–C, MSX3 interacts with promoters of Pparg, Stat6, and Jak3 in primary cultured microglia. The enrichment of MSX3 on the promoter of the genes indicated was determined using ChIP qPCR in MSX3-overexpressed microglia 72 h after transduction, confirming a direct interaction between MSX3 and promoters of Pparg (A), Stat6 (B), and Jak3 (C). In contrast, no direct interaction between MSX3 and promoters of Jak1, Ptp1b, or Cebpb was detected. The data are shown as the means ± SEM of three independent experiments. **p < 0.01 versus the IgG control. D–F, qPCR analysis of PPARγ, STAT6, and JAK3 mRNA in microglia. G–I, Immunoblot analysis of the expression of PPARγ, phospho-STAT6, STAT6, and JAK3 in MSX3 RNAi microglia with or without IL-4 stimulation and their controls. J–L, Immunoblot analysis of the expression of PPARγ, phospho-STAT6, STAT6, and JAK3 in MSX3-overexpressed microglia and its control. Scanning densitometry was quantified and normalized to the control on the same Western blots. GAPDH expression was analyzed from the same samples as an internal control for all Western blots. Representative blots are shown from three independent experiments. The data are shown as means ± SEM of three independent experiments. *p < 0.05; **p < 0.01; ***p < 0.005 versus control, as indicated. AU, Arbitrary units.

  1. The Journal of Neuroscience vol. 35 no. 16 6350-6365
Responses to This Article
Be the first to respond to this article
View Similar Articles
Similar articles in this journal»
    Advertisement