Figure 3.
Figure 3. Transient thrombocytopenia partially protects CCl4-induced liver fibrosis. (A) Experimental protocol showing IgG vs anti-GP-1bα (α-GP1bα) injection times and the CCl4 challenge time points (indicated by arrows) for the duration of the 36-day experiment. (B) Platelet counts showed marked thrombocytopenia in WT mice 1 day after α-GP1bα antibody administration (P = .01 for isotype-matched IgG vs α-GP1bα injections). (C) Picrosirius red staining images at 36 days (both light and polarized light microscopy) showed fibrotic areas in liver sections of WT mice pretreated with IgG or α-GP1bα and then subjected to CCl4 challenge. (D) Quantification of liver fibrosis showed that mice pretreated with α-GP1bα (n = 7) had significantly less fibrosis than those pretreated with IgG (n = 5; P = .01) at 36 days.

Transient thrombocytopenia partially protects CCl4-induced liver fibrosis. (A) Experimental protocol showing IgG vs anti-GP-1bα (α-GP1bα) injection times and the CCl4 challenge time points (indicated by arrows) for the duration of the 36-day experiment. (B) Platelet counts showed marked thrombocytopenia in WT mice 1 day after α-GP1bα antibody administration (P = .01 for isotype-matched IgG vs α-GP1bα injections). (C) Picrosirius red staining images at 36 days (both light and polarized light microscopy) showed fibrotic areas in liver sections of WT mice pretreated with IgG or α-GP1bα and then subjected to CCl4 challenge. (D) Quantification of liver fibrosis showed that mice pretreated with α-GP1bα (n = 7) had significantly less fibrosis than those pretreated with IgG (n = 5; P = .01) at 36 days.

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