Fig 1: Immunohistochemistry: the liver was collected from mice sacrificed 6 h after LPS injection, sectioned, and stained for H&E ((A,B), bar = 100 µm), VWF ((C,D), bar = 100 µm), and fibrin ((E,F), bar = 20 µm) on an automatic histochemistry-staining platform. Images are representative of sections from 25 mice in each experimental group.
Fig 2: Plasma VWF levels: plasma VWF was measured by a commercial ELISA kit 24 h after LPS challenge. LPS resulted in a significant increase in plasma VWF antigen. The increase was similar for mice receiving rhADAMTS-13 and those receiving vehicle control (n = 6/group, one-way ANOVA, n = 28).
Fig 3: Plasma VWF concentrations. Open column, MCT-treated group; closed column, control. Data are expressed as mean ± SD (n = 7). #, p < 0.02 vs. control 0 h; *, p < 0.05 vs. MCT group 0 h or control 24 h.
Fig 4: Role of GSNOR in SARS-CoV-2 SP (S1 domain)-induced lung diseases. Male WT (C57BL/6) and GSNOR knockout (KO) mice were administered the S1 domain of SARS-CoV-2 spike protein (S1) intranasally on a daily basis for 10 days and blood levels of TNFα (Ai), lung infiltrations of CD11c+ macrophages and Ly6G + neutrophils (Aii, iii), extravasation of Evans blue into the lungs (Bi), lung edema (Bii), lung vascular (CD31) expression of ICAM-1 (Ci) and VCAM-1 (Cii), blood levels of vWF and fibrinogen (Di, ii), lung deposition of fibrin (Ei, ii) were analyzed. The bar graph represents the mean ± standard error mean and the scatter dot plot represents an individual data point. *p < 0.05; **p ≤ 0.01, ***p ≤ 0.001 vs control mice and+p < 0.05; ++ p ≤ 0.01, +++ p ≤ 0.001 vs as indicated. N.S.: not significant.
Fig 5: Plasma VWF (A2) concentrations. Open column, MCT-treated group; closed column, control. Data are expressed as mean ± SD (n = 7). Data are expressed as mean ± SD (n = 7). *, p < 0.001 vs. MCT group 0 h or control 48 h.
Supplier Page from Abcam for Mouse Von Willebrand Factor A2 ELISA Kit