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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >S100A9 promotes human lung fibroblast cells activation through receptor for advanced glycation end-product-mediated extracellular-regulated kinase 1/2, mitogen-activated protein-kinase and nuclear factor-κB-dependent pathways
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S100A9 promotes human lung fibroblast cells activation through receptor for advanced glycation end-product-mediated extracellular-regulated kinase 1/2, mitogen-activated protein-kinase and nuclear factor-κB-dependent pathways

机译：S100A9通过受体的高级糖基化终产物介导的细胞外调节激酶1/2，促分裂原激活的蛋白激酶和核因子-κB依赖性途径促进人肺成纤维细胞活化

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S100A9 belongs to the S100 family of calcium-binding proteins and plays a key role in many inflammatory conditions. Recent studies have found that S100A9 was elevated significantly in the bronchoalveolar lavage fluid of idiopathic pulmonary fibrosis patients, and might be a biomarker for fibrotic interstitial lung diseases. However, the exact function of S100A9 in pulmonary fibrosis needs further studies. We performed this study to investigate the effect of S100A9 on human embryo lung fibroblast (HLF) proliferation and production of cytokines and collagen, providing new insights into the possible mechanism. S100A9 promoted proliferation of fibroblasts and up-regulated expression of both proinflammatory cytokines interleukin (IL)-6, IL-8, IL-1β and collagen type III. S100A9 also induced HLF cells to produce α-smooth muscle actin (α-SMA) and receptor for advanced glycation end-product (RAGE). In addition, S100A9 caused a significant increase in extracellular-regulated kinase (ERK)1/2 mitogen-activated protein kinase (MAPK) phosphorylation, while the status of p38 and c-Jun N-terminal kinase (JNK) phosphorylation remained unchanged. Treatment of cells with S100A9 also enhanced nuclear factor kappa B (NF-κB) activation. RAGE blocking antibody pretreatment inhibited the S100A9-induced cell proliferation, cytokine production and pathway phosphorylation. S100A9-mediated cell activation was suppressed significantly by ERK1/2 MAPK inhibitor and NF-κB inhibitor. In conclusion, S100A9 promoted HLF cell growth and induced cells to secret proinflammatory cytokines and collagen through RAGE signalling and activation of ERK1/2 MAPK and NF-κB pathways.
机译：S100A9属于S100钙结合蛋白家族，在许多炎性疾病中起关键作用。最近的研究发现，特发性肺纤维化患者的支气管肺泡灌洗液中S100A9显着升高，可能是纤维化间质性肺疾病的生物标志物。但是，S100A9在肺纤维化中的确切功能尚需进一步研究。我们进行了这项研究，以研究S100A9对人胚肺成纤维细胞（HLF）增殖以及细胞因子和胶原蛋白产生的影响，从而为可能的机制提供了新见解。 S100A9促进成纤维细胞的增殖，并上调促炎细胞因子白介素（IL）-6，IL-8，IL-1β和III型胶原蛋白的表达。 S100A9还诱导HLF细胞产生α平滑肌肌动蛋白（α-SMA）和晚期糖基化终产物（RAGE）的受体。此外，S100A9引起细胞外调节激酶（ERK）1/2丝裂原活化蛋白激酶（MAPK）磷酸化的显着增加，而p38和c-Jun N端激酶（JNK）磷酸化的状态保持不变。用S100A9处理细胞还增强了核因子κB（NF-κB）的激活。 RAGE封闭抗体预处理可抑制S100A9诱导的细胞增殖，细胞因子生成和途径磷酸化。 S100A9介导的细胞活化被ERK1 / 2 MAPK抑制剂和NF-κB抑制剂显着抑制。总之，S100A9通过RAGE信号传导和ERK1 / 2 MAPK和NF-κB通路的活化，促进HLF细胞生长并诱导细胞分泌促炎细胞因子和胶原。

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