Objective(s): This study aims to investigate the pathogenicity and possible mechanisms of S100A9 function in mice models of scleroderma. Materials and Methods: The content of S100A9 in the skin tissues of mice with scleroderma was determined. Different concentrations of bleomycin (BLM) and S100A9 were subcutaneously injected into the backs of mice simultaneously, and then pathological changes in the skin of these mice were monitored. Specifically, the levels of inflammatory cytokines and alpha smooth muscle actin (a-SMA), the activation of extracellular regulated kinase 1/2 (ERK1/2), mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-kappa B) pathways, and the expression of the receptor for advanced glycation end-product (RAGE) in the skin were determined. Results: The content of S100A9 in the skin tissues of mice with scleroderma was determined. Different concentrations of BLM and S100A9 were subcutaneously injected into the backs of mice simultaneously, and then pathological changes in the skin of these mice were monitored. Specifically, the levels of inflammatory cytokines and alpha smooth muscle actin (alpha-SMA), the activation of extracellular regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-kappa B) pathways, and the expression of the receptor for advanced glycation end-product (RAGE) in the skin were determined. Conclusion: S100A9 aggravates dermal fibrosis in BLM-induced scleroderma (BIS) mice, and its mechanisms might be mediated by RAGE, ERK1/2, and NF-.B pathway.
[1]Nanjing Univ Med Sch, Affiliated Hosp, Nanjing Drum Tower Hosp, Dept Rheumatol & Immunol, 321 Zhongshan Rd, Nanjing 210008, Jiangsu, Peoples R China.
[2]Fudan Univ, Huashan Hosp, Div Rheumatol, Shanghai 200040, Peoples R China.
[3]Fudan Univ, State Key Lab Genet Engn, Shanghai 200433, Peoples R China.
[4]Fudan Univ, Minist Educ Key Lab Contemporary Anthropol, Sch Sci, Shanghai 200433, Peoples R China.
(8.0+极速模式)