Fig. 4

IL-1α acts through proteolytic processing of perlecan. Mice lacking the LG3 fragment of perlecan do not sustain the same protection following IV IL-1α treatment showing larger infarct volumes overall than WT controls on PSD 3 (a). Quantification of infarct volumes obtained from cresyl violet stains (b) one-way ANOVA ####p < 0.0001 WT IL-1α vs. pln KO IL-1α; ****p < 0.0001 WT PBS vs. WT IL-1α (n = 7 per group). IL-1α treatment increases mRNA expression of cathepsin B and perlecan in vitro. Mouse brain endothelial cells treated with 1 ng/mL IL-1α for 4 h express more cathepsin B (c) and perlecan (d) mRNA. This effect is abolished for the production of cathepsin B but not perlecan upon treatment with IL-1RA. One-way ANOVA *p < 0.05 IL-1α vs. Veh conditions. Data are the mean ± SEM