Fig. 3.

Fibrin–CD11b interaction regulates innate immune programs in TBI. (A) PCA analysis of RNA-seq analysis of microglia from Fgg^γ390–396A, WT, and sham mice. 1 day (1d) after injury; 7 days (7d) after injury. Data are from n = 3 independent samples per group. (B) Volcano plot of DEGs from RNA-seq analysis of sorted microglia from Fgg^γ390–396A and WT mice 1d after injury. Comparison between DEGs in microglia from 1d Fgg^γ390–396A vs. 1d WT mice is shown. Dots depict average log₂ fold change (FC) and -log₁₀ adjusted P values by significance cutoff (abs(log₂FC) > 1, adjusted P value < 0.1 with Wald test followed by Benjamini-Hochberg multiple test correction). Top DEGs are shown. Data are from n = 3 independent samples per group. (C, D) GSEA plots (C) or coexpression networks (D) of downregulated gene ontology (GO) terms in 1d Fgg^γ390–396A vs. 1d WT microglia. (E) Dot plot of selected gene markers expressed by microglia from sham, 7d WT, and 7d Fgg^γ390–396A mice. Data are from n = 3 independent samples per group. nd, not detected. (F) Volcano plot of DEGs from RNA-seq analysis of sorted infiltrating myeloid cells from 1d Fgg^γ390–396A and 1d WT mice. Dots depict average log₂FC and -log₁₀ adjusted P values by significance cutoff (abs(log₂FC) > 1, adjusted P value < 0.1 with Wald test followed by Benjamini-Hochberg multiple test correction). Top DEGs are shown. Data are from n = 3 independent samples per group. (G) GSEA dot plot of GO terms significantly upregulated in infiltrating myeloid cells from 1d Fgg^γ390–396A vs. 1d WT mice