Xue Xu - Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing ۲۱۰۰۰۸, Jiangsu, China
Zhiyong Chen - Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing ۲۱۰۰۰۸, Jiangsu, China
Xiaoxia Zhu - Division of Rheumatology, Huashan Hospital, Fudan University, Shanghai ۲۰۰۰۴۰, China
Dandan Wang - Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing ۲۱۰۰۰۸, Jiangsu, China
Jun Liang - Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing ۲۱۰۰۰۸, Jiangsu, China
Cheng Zhao - Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing ۲۱۰۰۰۸, Jiangsu, China
Xuebing Feng - Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing ۲۱۰۰۰۸, Jiangsu, China
Jiucun Wang - State Key Laboratory of Genetic Engineering and Ministry of Education Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University, Shanghai ۲۰۰۴۳۳, China
Hejian Zou - Division of Rheumatology, Huashan Hospital, Fudan University, Shanghai ۲۰۰۰۴۰, China
Lingyun Sun - Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing ۲۱۰۰۰۸, Jiangsu, China

Objective(s): This study aims to investigate the pathogenicity and possible mechanisms of S۱۰۰A۹ function in mice models of scleroderma. Materials and Methods: The content of S۱۰۰A۹ in the skin tissues of mice with scleroderma was determined. Different concentrations of bleomycin (BLM) and S۱۰۰A۹ 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 (α-SMA), the activation of extracellular regulated kinase ۱/۲ (ERK۱/۲), mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) pathways, and the expression of the receptor for advanced glycation end-product (RAGE) in the skin were determined. Results: The content of S۱۰۰A۹ in the skin tissues of mice with scleroderma was determined. Different concentrations of BLM and S۱۰۰A۹ 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 (α-SMA), the activation of extracellular regulated kinase ۱/۲ (ERK۱/۲) mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) pathways, and the expression of the receptor for advanced glycation end-product (RAGE) in the skin were determined. Conclusion: S۱۰۰A۹ aggravates dermal fibrosis in BLM-induced scleroderma (BIS ) mice, and its mechanisms might be mediated by RAGE, ERK۱/۲, and NF-κB pathway.

S۱۰۰A۹, Scleroderma, Bleomycin, RAGE, ERK۱/۲ MAPK, NF-κB