Fig. 5

Transcriptomic analysis of selected TF families in BV-2 microglial cells. a Heat map represents differential expression of NF-κB, STAT, KLF, and IRF TF families, as well as other TF genes, (P <0.001) at 2 and 4 h after Poly (I:C) and LPS stimulation in BV-2 microglial cells. b UCSC browser images representing normalized RNA-seq read densities for TF expression after Poly (I:C) (left panel) and LPS (right panel) stimulation in BV-2 microglia cells compared with controls. c Patterns of transcription factor motif enrichments within the promoters of the genes in Poly (I:C)- and LPS-stimulated BV-2 microglia cells. d, e The activity of highly connected positive regulators of the inflammatory genes IRF1, IRF7, JUNB, NF-κBIA, STAT1, and CREPD led to the activation of this network, as assessed using the IPA molecule activity predictor in Poly (I:C)- and LPS-stimulated BV-2 microglia cells. f, g Results of the GO term analysis using DAVID on genes that were regulated by NF-κBIA and STAT1 in Poly (I:C) and LPS response BV-2 microglial cells respectively. (H, I) The IL1A, CCL7 and CCL2 genes were significantly down-regulated in NF-κB inhibitor Bay 11-7082 (10 μM)-treated BV-2 microglial cells at 2 h and 4 h under inflammatory conditions (Poly (I:C) 5 μg/ml and LPS 10 ng/mL). Gene expression was normalized to GAPDH transcript levels. *P <0.05 and **P <0.001 compared with the control. The data represent three independent experiments