Extended Data Fig. 5: Downregulation of CD82 and upregulation of FARP1-Cdc42 signaling as anti-inflammation therapeutic strategies.
(a) Western blot analysis on the lysates of MLECs isolated from Ctrl., Cd82ΔEC, and Cd82ΔEC;Cdc42ΔEC mice. (b)-(c) Histochemistry (H-E staining) (b) and immunofluorescence (CD45 staining) (c) analyses on lung sections of the Control, Cd82ΔEC, and Cd82ΔEC;Cdc42ΔEC mice treated with LPS (5 mg/kg) for 18 h described in Fig. 3i. (d) Quantifications of acute lung injury (violin plot), Evans Blue extravasation or vascular leakage (mean±SD), and leukocyte infiltration of the lungs (violin plot) from Control, Cd82ΔEC, and Cd82ΔEC;Cdc42ΔEC mice, n=10 mice per group. (e) Western blot analysis of FARP1 in the HUVECs transfected with control and FARP1 siRNA. (f) Efficiency of in vitro FARP1 delivery and expression with endothelium-specific hADv5 viruses. The bEnd.3 cells infected by the viruses encoding control or FARP1 were examined in Western blot. (g-h) Histochemistry analysis (H-E staining) (g) and immunofluorescence analysis (CD45 staining) (h) on lung sections of the mice delivered with HAdV5-control (HAdV5-Vector) or HAdV5-FARP1 viruses. Ten days after the viral injection, the mice were challenged with LPS (5 mg/kg, i.p.) for 18 h prior to euthanasia. (i) Quantifications of acute lung injury (violin plot), vascular leakage or Evans Blue extravasation (mean±SD), and leukocyte infiltration of the lungs (violin plot) from the mice administered with HAdV5-control or HAdV5-FARP1 viruses, n=6 mice/ group.
