ArticleClinical and experimental immunology2013
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.
Article in Clinical and experimental immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 67 citations in OpenAlex.
- The Role of Neutrophil, Monocyte and Macrophage Calprotectin and S100A12 in the Fibrotic Process.Biomolecules · 2026Review
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- Calprotectin inhibition attenuates silica-induced lung fibrosis.Inflammopharmacology · 2025Article
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- Beyond the clot: how the biomolecular landscape of platelet-rich fibrin directs fibroblast functions.Frontiers in oral health · 2025Review
- Microarray analysis of gene expression in lung tissues of indium-exposed rats: possible roles of S100 proteins in lung diseases.Archives of toxicology · 2025Article
- Fibroblast-Adipocyte Lineage Cell Interactions Result in Differential Production of Extracellular Matrix Proteins.Cellular and molecular bioengineering · 2024Article
- Calprotectin is regulated by IL-17A and induces steroid hyporesponsiveness in asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Dysregulated S100A9 Expression Impairs Matrix Deposition in Chronic Wounds.International journal of molecular sciences · 2024Article
- The RAGE Axis: A Relevant Inflammatory Hub in Human Diseases.Biomolecules · 2024Review
- High S100A9 level predicts poor survival, and the S100A9 inhibitor paquinimod is a candidate for treating idiopathic pulmonary fibrosis.BMJ open respiratory research · 2024Article
- S100 Calcium-Binding Protein A9, a Potential Novel Diagnostic Biomarker for Idiopathic Pulmonary Fibrosis.Journal of Korean medical science · 2024Article
- S100 calcium-binding protein A9 promotes skin regeneration through toll-like receptor 4 during tissue expansion.Burns & trauma · 2023Article
- Receptor for Advanced Glycation End Products (RAGE): A Pivotal Hub in Immune Diseases.Molecules (Basel, Switzerland) · 2022Review
- Calprotectin in Lung Diseases.International journal of molecular sciences · 2021Review
- Serum calprotectin as new biomarker for disease severity in idiopathic pulmonary fibrosis: a cross-sectional study in two independent cohorts.BMJ open respiratory research · 2021Article
- Inhibitory Effect of Paquinimod on a Murine Model of Neutrophilic Asthma Induced by Ovalbumin with Complete Freund's Adjuvant.Canadian respiratory journal · 2021Article
- The S100 Protein Family as Players and Therapeutic Targets in Pulmonary Diseases.Pulmonary medicine · 2021Review
- S100A8 and S100A9 promote endothelial cell activation through the RAGE‑mediated mammalian target of rapamycin complex 2 pathway.Molecular medicine reports · 2020Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
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.
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