Figure 5

Stat3 deletion rescues hIL-1α cTg phenotypes. hIL-1α cTg (cTg) mice were crossed with Stat3 floxed (Stat3 cKO) mice to yield cTg/Stat3 cKO mice. PolyI-PolyC was injected into eight-week-old Ctl, cTg or cTg/Stat3 cKO mice, and ankle thickness evaluated at indicated time points (a). Data represent mean ankle thickness ± SD (n = 3 for control; n = 3 for cTg mice; n = 5 for cTg/Stat3 cKO; ^**P < 0.01, ^*P < 0.05, NS not significant, cTg vs cTg/Stat3 cKO). Three weeks after PolyI-PolyC injection, ankle joints (b–d) and peripheral blood (e) were collected. Ankle tissue specimens from all three genotypes were stained with HE (upper panels) or safranin O and methyl green (lower panels) (b), and the safranin O-positive articular cartilage area (b) and Mankin scores were evaluated (c). Data in (b,c) represent mean safranin O-positive area (b) (n = 3 for control; n = 3 for cTg mice; n = 4 for cTg + Stat3 cKO mice; ^*P < 0.05, ^**P < 0.01) or Mankin score (c) ± SD (n = 5 for control; n = 3 for cTg mice; n = 3 for cTg + Stat3 cKO mice; ^**P < 0.01, ^***P < 0.001). Bar, 100 µm. Destruction of ankle bone from Ctl, cTg or cTg + Stat3 cKO mice was evaluated using micro-CT (d). White blood cell (WBC), hemoglobin (Hb) and platelet (Plt) counts in peripheral blood were scored (e). Data represent mean WBC, Hb or Plt ± SD (n = 5 for control; n = 4 for cTg mice; n = 5 for cTg/Stat3 cKO; ^***P < 0.001, ^**P < 0.01, ^*P < 0.05, NS not significant).