Roles for ST2 in the pathogenesis of HA in F8em1−/− mice. (A) Graphical illustration of IL-33 binding to IL-33 receptor (ST2 and IL-1RAP) and resulting cell activation pathway. (B) Enzyme-linked immunosorbent assay quantification of soluble ST2 (sST2) and IL-33 in plasma of F8em1−/− mice after needle injury. Data presented as mean ± SEM (n = 5-9 mice per group) and the Student t test was used for statistical analysis between groups at each time point. (C) Graphical illustration showing the generation of double F8em1−/−/Il1rl1−/− mice. (D) FVIII:C FVIII activity in plasma of WT, Il1rl1−/−, F8em1−/−, and F8em1−/−/Il1rl1−/− mice (n = 3-4). (E) Kaplan-Meier curves of comparable survival of male F8em1−/− and F8em1−/−/Il1rl1−/− mice from birth to 200 days (n = 100 mice per group). (F) Increase in knee joint diameter (percentage) of F8em1−/− and F8em1−/−/Il1rl1−/− mice after needle injury. Red crosses indicate deaths of F8em1−/− mice, and blue crosses indicate deaths of F8em1−/−/Il1rl1−/− mice. Data are from triplicate experiments presented as mean ± SEM (24-27 mice per group). (G) Representative Prussian blue staining and hemosiderin (indicated by arrow) and deposition scores. (H) H&E-stained joint sections showing the synovium (indicated by x----x) and synovitis scores. (I) Safranin O staining of the cartilage in joints and degradation scores. Histology data are mean ± SEM (8-10 mice per group). The area under the curve (AUC) of joint swelling was calculated for individual mice, and the Student t test was used for statistical analysis between group AUC or tissue histology scores. ∗P ≤ .05; ∗∗P ≤ .01. KO, knockout; ns, nonsignificant.
Figure 6.

Roles for ST2 in the pathogenesis of HA in F8em1−/− mice. (A) Graphical illustration of IL-33 binding to IL-33 receptor (ST2 and IL-1RAP) and resulting cell activation pathway. (B) Enzyme-linked immunosorbent assay quantification of soluble ST2 (sST2) and IL-33 in plasma of F8em1−/− mice after needle injury. Data presented as mean ± SEM (n = 5-9 mice per group) and the Student t test was used for statistical analysis between groups at each time point. (C) Graphical illustration showing the generation of double F8em1−/−/Il1rl1−/− mice. (D) FVIII:C FVIII activity in plasma of WT, Il1rl1−/−, F8em1−/−, and F8em1−/−/Il1rl1−/− mice (n = 3-4). (E) Kaplan-Meier curves of comparable survival of male F8em1−/− and F8em1−/−/Il1rl1−/− mice from birth to 200 days (n = 100 mice per group). (F) Increase in knee joint diameter (percentage) of F8em1−/− and F8em1−/−/Il1rl1−/− mice after needle injury. Red crosses indicate deaths of F8em1−/− mice, and blue crosses indicate deaths of F8em1−/−/Il1rl1−/− mice. Data are from triplicate experiments presented as mean ± SEM (24-27 mice per group). (G) Representative Prussian blue staining and hemosiderin (indicated by arrow) and deposition scores. (H) H&E-stained joint sections showing the synovium (indicated by x----x) and synovitis scores. (I) Safranin O staining of the cartilage in joints and degradation scores. Histology data are mean ± SEM (8-10 mice per group). The area under the curve (AUC) of joint swelling was calculated for individual mice, and the Student t test was used for statistical analysis between group AUC or tissue histology scores. ∗P ≤ .05; ∗∗P ≤ .01. KO, knockout; ns, nonsignificant.

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