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The autocrine CXCR4/CXCL12 axis contributes to lung fibrosis through modulation of lung fibroblast activity
The C-X-C Motif Chemokine Receptor 4/C-X-C Motif Chemokine Ligand 12 (CXCR4/CXCL12) axis has been implicated in the pathogenesis of pulmonary fibrosis. However, the mechanisms governing this remain to be determined. The current study demonstrated that human lung fibroblasts (HLFs) exhibit high CXCL1...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7027131/ https://www.ncbi.nlm.nih.gov/pubmed/32104240 http://dx.doi.org/10.3892/etm.2020.8433 |
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author | Li, Fei Xu, Xuefeng Geng, Jing Wan, Xuan Dai, Huaping |
author_facet | Li, Fei Xu, Xuefeng Geng, Jing Wan, Xuan Dai, Huaping |
author_sort | Li, Fei |
collection | PubMed |
description | The C-X-C Motif Chemokine Receptor 4/C-X-C Motif Chemokine Ligand 12 (CXCR4/CXCL12) axis has been implicated in the pathogenesis of pulmonary fibrosis. However, the mechanisms governing this remain to be determined. The current study demonstrated that human lung fibroblasts (HLFs) exhibit high CXCL12 expression and also exhibit high expression of its corresponding receptor CXCR4. Exogenous CXCL12 was revealed to significantly promote the migration and proliferation of HLFs, and potentiate CXCR4 expression. These effects were demonstrated to be inhibited by AMD3100, which is an antagonist of CXCR4. Lung and bronchoalveolar lavage fluid CXCR4 and CXCL12 expression was upregulated by in vivo bleomycin administration, which was partially inhibited by pre-treatment with AMD3100. AMD3100 also reduced lung collagen content in the bleomycin model. Inhibiting CXCR4 was indicated to ameliorate the lung compliance and resistance of pulmonary fibrosis. In conclusion, the results of the present study suggested that autocrine CXCR4/CXCL12 axis is an important mechanism underlying the pathogenesis of idiopathic pulmonary fibrosis, and may serve as a potential therapeutic target that can be used in the treatment of pulmonary disease. |
format | Online Article Text |
id | pubmed-7027131 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-70271312020-02-26 The autocrine CXCR4/CXCL12 axis contributes to lung fibrosis through modulation of lung fibroblast activity Li, Fei Xu, Xuefeng Geng, Jing Wan, Xuan Dai, Huaping Exp Ther Med Articles The C-X-C Motif Chemokine Receptor 4/C-X-C Motif Chemokine Ligand 12 (CXCR4/CXCL12) axis has been implicated in the pathogenesis of pulmonary fibrosis. However, the mechanisms governing this remain to be determined. The current study demonstrated that human lung fibroblasts (HLFs) exhibit high CXCL12 expression and also exhibit high expression of its corresponding receptor CXCR4. Exogenous CXCL12 was revealed to significantly promote the migration and proliferation of HLFs, and potentiate CXCR4 expression. These effects were demonstrated to be inhibited by AMD3100, which is an antagonist of CXCR4. Lung and bronchoalveolar lavage fluid CXCR4 and CXCL12 expression was upregulated by in vivo bleomycin administration, which was partially inhibited by pre-treatment with AMD3100. AMD3100 also reduced lung collagen content in the bleomycin model. Inhibiting CXCR4 was indicated to ameliorate the lung compliance and resistance of pulmonary fibrosis. In conclusion, the results of the present study suggested that autocrine CXCR4/CXCL12 axis is an important mechanism underlying the pathogenesis of idiopathic pulmonary fibrosis, and may serve as a potential therapeutic target that can be used in the treatment of pulmonary disease. D.A. Spandidos 2020-03 2020-01-08 /pmc/articles/PMC7027131/ /pubmed/32104240 http://dx.doi.org/10.3892/etm.2020.8433 Text en Copyright: © Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Li, Fei Xu, Xuefeng Geng, Jing Wan, Xuan Dai, Huaping The autocrine CXCR4/CXCL12 axis contributes to lung fibrosis through modulation of lung fibroblast activity |
title | The autocrine CXCR4/CXCL12 axis contributes to lung fibrosis through modulation of lung fibroblast activity |
title_full | The autocrine CXCR4/CXCL12 axis contributes to lung fibrosis through modulation of lung fibroblast activity |
title_fullStr | The autocrine CXCR4/CXCL12 axis contributes to lung fibrosis through modulation of lung fibroblast activity |
title_full_unstemmed | The autocrine CXCR4/CXCL12 axis contributes to lung fibrosis through modulation of lung fibroblast activity |
title_short | The autocrine CXCR4/CXCL12 axis contributes to lung fibrosis through modulation of lung fibroblast activity |
title_sort | autocrine cxcr4/cxcl12 axis contributes to lung fibrosis through modulation of lung fibroblast activity |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7027131/ https://www.ncbi.nlm.nih.gov/pubmed/32104240 http://dx.doi.org/10.3892/etm.2020.8433 |
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