Research Paper Volume 14, Issue 14 pp 5669—5680

Transcription factor KLF4 regulated STAT1 to promote M1 polarization of macrophages in rheumatoid arthritis

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Figure 5. Effect of KLF4 on the pathology of RA mice (n=3). (A) In Cartilage surface and transitional layer, H&E staining of mouse joint tissues, IHC staining of STAT1 and Safranin O-fast green staining results (n=5). H&E staining results showed that, KLF4 further induced cartilage injury, and obvious joint tissue injury was observed in mice, which was more severe than that of RA group. KLF4 induced STAT1 expression in joint tissues, and the expression in RA+KLF4 group was markedly higher than that in RA group. Safranin O-fast green staining revealed diffuse staining in RA+KLF4 group, which suggested the more severe cartilage injury than that of RA group. (B) Mouse clinical pathological score (n=10). RA group had a remarkably higher score than Control group, and RA+KLF4 group had a markedly higher score than RA group. *P<0.05 compared with Control group, #P<0.05 compared with RA group. (C) Expression of inflammatory factors in mouse joint tissues (n=5). The inflammatory factor levels in RA group were markedly higher than those in Control group, while those in RA+KLF4 group were further up-regulated, higher than those of RA group. *P<0.05 compared with Control group, #P<0.05 compared with RA group. (D, E) Expression of JAK1-STAT1 signal proteins (n=5). The JAK1-STAT1 signals in RA group were activated, and their protein and phosphorylation levels were remarkably up-regulated, higher than those of Control group. Meanwhile, the protein levels in RA+KLF4 group were further up-regulated, higher than those of RA group. *P<0.05 compared with Control group, #P<0.05 compared with RA group.