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This study aimed to reveal the mechanism of transcription factor Kruppel-like factor 4 (KLF4) in regulating M1 polarization of macrophages in rheumatoid arthritis (RA) in order to induce inflammatory response. The results suggested that KLF4 overexpression promoted the M1 polarization of RAW 264.7 cells, increased STAT1 expression and up-regulated the phosphorylation level. After KLF4 silencing, the M1 polarization level was down-regulated. Besides, the induced M1 macrophages were co-cultured with articular chondrocytes. KLF4 overexpression further aggravated chondrocyte injury, increased the cell apoptosis rate and activated the inflammatory injury. However, pretreatment with STAT1 inhibitor Cerulomycin resisted the effect of KLF4, and significantly suppressed STAT1 expression and M1 polarization of cells. KLF4 overexpression aggravated synovial tissue injury in mouse joints, up-regulated the expression of inflammatory factors, and increased the levels of CD86 and STAT1. It was discovered that transcription factor KLF4 promoted the transcription of STAT1 to regulate the M1 polarization of macrophages, thus aggravating the progression of RA and inflammatory response.

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