S100A9通过激活ERK1/2丝裂原活化蛋白激酶（MAPK）和核因子κB（NF-κB）信号通路加重博来霉素诱导的小鼠皮肤纤维化。
S100A9 aggravates bleomycin-induced dermal fibrosis in mice via activation of ERK1/2 MAPK and NF-κB pathways.
作者信息
Xu Xue, Chen Zhiyong, Zhu Xiaoxia, Wang Dandan, Liang Jun, Zhao Cheng, Feng Xuebing, Wang Jiucun, Zou Hejian, Sun Lingyun
机构信息
Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing 210008, Jiangsu, China.
Division of Rheumatology, Huashan Hospital, Fudan University, Shanghai 200040, China.
出版信息
Iran J Basic Med Sci. 2018 Feb;21(2):194-201. doi: 10.22038/IJBMS.2018.19987.5255.
OBJECTIVES
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 (α-SMA), the activation of extracellular regulated kinase 1/2 (ERK1/2), 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 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 (α-SMA), the activation of extracellular regulated kinase 1/2 (ERK1/2) 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
S100A9 aggravates dermal fibrosis in BLM-induced scleroderma (BIS) mice, and its mechanisms might be mediated by RAGE, ERK1/2, and NF-κB pathway.
目的
本研究旨在探讨硬皮病小鼠模型中S100A9功能的致病性及可能机制。
材料与方法
测定硬皮病小鼠皮肤组织中S100A9的含量。将不同浓度的博来霉素（BLM）和S100A9同时皮下注射到小鼠背部，然后监测这些小鼠皮肤的病理变化。具体而言，测定皮肤中炎性细胞因子和α平滑肌肌动蛋白（α-SMA）的水平、细胞外调节激酶1/2（ERK1/2）、丝裂原活化蛋白激酶（MAPK）和核因子-κB（NF-κB）信号通路的激活情况，以及晚期糖基化终末产物受体（RAGE）在皮肤中的表达。
结果
测定了硬皮病小鼠皮肤组织中S100A9的含量。将不同浓度的博来霉素（BLM）和S100A9同时皮下注射到小鼠背部，然后监测这些小鼠皮肤的病理变化。具体而言，测定皮肤中炎性细胞因子和α平滑肌肌动蛋白（α-SMA）的水平、细胞外调节激酶1/2（ERK1/2）、丝裂原活化蛋白激酶（MAPK）和核因子-κB（NF-κB）信号通路的激活情况，以及晚期糖基化终末产物受体（RAGE）在皮肤中的表达。
结论
S100A9加重博来霉素诱导的硬皮病（BIS）小鼠的皮肤纤维化，其机制可能由RAGE、ERK1/2和NF-κB信号通路介导。
Zotero 插件