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1000 Titel
  • Extracellular CIRP Induces an Inflammatory Phenotype in Pulmonary Fibroblasts via TLR4
1000 Autor/in
  1. Bolourani, Siavash |
  2. Sari, Ezgi |
  3. Brenner, Max |
  4. Wang, Ping |
1000 Verlag
  • Frontiers Media S.A.
1000 Erscheinungsjahr 2021
1000 Publikationstyp
  1. Artikel |
1000 Online veröffentlicht
  • 2021-07-23
1000 Erschienen in
1000 Quellenangabe
  • 12:721970
1000 Copyrightjahr
  • 2021
1000 Embargo
  • 2022-01-25
1000 Lizenz
1000 Verlagsversion
  • https://doi.org/10.3389/fimmu.2021.721970 |
  • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8342891/ |
1000 Publikationsstatus
1000 Begutachtungsstatus
1000 Abstract/Summary
  • <jats:p>Extracellular cold-inducible RNA-binding protein (eCIRP), a new damage-associated molecular pattern (DAMP), has been recently shown to play a critical role in promoting the development of bleomycin-induced pulmonary fibrosis. Although fibroblast activation is a critical component of the fibrotic process, the direct effects of eCIRP on fibroblasts have never been examined. We studied eCIRP’s role in the induction of inflammatory phenotype in pulmonary fibroblasts and its connection to bleomycin-induced pulmonary fibrosis in mice. We found that eCIRP causes the induction of proinflammatory cytokines and differentially expression-related pathways in a TLR4-dependent manner in pulmonary fibroblasts. Our analysis further showed that the accessory pathways MD2 and Myd88 are involved in the induction of inflammatory phenotype. In order to study the connection of the enrichment of these pathways in priming the microenvironment for pulmonary fibrosis, we investigated the gene expression profile of lung tissues from mice subjected to bleomycin-induced pulmonary fibrosis collected at various time points. We found that at day 14, which corresponds to the inflammatory-to-fibrotic transition phase after bleomycin injection, TLR4, MD2, and Myd88 were induced, and the transcriptome was differentially enriched for genes in those pathways. Furthermore, we also found that inflammatory cytokines gene expressions were induced, and the cellular responses to these inflammatory cytokines were differentially enriched on day 14. Overall, our results show that eCIRP induces inflammatory phenotype in pulmonary fibroblasts in a TLR4 dependent manner. This study sheds light on the mechanism by which eCIRP induced inflammatory fibroblasts, contributing to pulmonary fibrosis.</jats:p>
1000 Sacherschließung
lokal Pulmonary Fibrosis/pathology [MeSH]
lokal Inflammation Mediators/metabolism [MeSH]
lokal Gene Expression [MeSH]
lokal Cytokines/metabolism [MeSH]
lokal bleomicyn
lokal inflammation
lokal Phenotype [MeSH]
lokal Disease Models, Animal [MeSH]
lokal Fibroblasts/metabolism [MeSH]
lokal Extracellular Space [MeSH]
lokal Immunology
lokal RNA-Binding Proteins/metabolism [MeSH]
lokal Animals [MeSH]
lokal Disease Susceptibility [MeSH]
lokal fibrosis
lokal Mice, Knockout [MeSH]
lokal Mice [MeSH]
lokal Pulmonary Fibrosis/metabolism [MeSH]
lokal Inflammation/complications [MeSH]
lokal fibroblast
lokal Inflammation/pathology [MeSH]
lokal eCIRP
lokal Inflammation/metabolism [MeSH]
lokal Signal Transduction [MeSH]
lokal Toll-Like Receptor 4/genetics [MeSH]
lokal Inflammation/etiology [MeSH]
lokal Pulmonary Fibrosis/etiology [MeSH]
lokal Gene Expression Profiling [MeSH]
lokal Toll-Like Receptor 4/metabolism [MeSH]
lokal Computational Biology/methods [MeSH]
1000 Liste der Beteiligten
  1. https://frl.publisso.de/adhoc/uri/Qm9sb3VyYW5pLCBTaWF2YXNo|https://frl.publisso.de/adhoc/uri/U2FyaSwgRXpnaQ==|https://frl.publisso.de/adhoc/uri/QnJlbm5lciwgTWF4|https://frl.publisso.de/adhoc/uri/V2FuZywgUGluZw==
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1000 Erstellt am 2024-05-21T14:35:00.973+0200
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1000 Zuletzt bearbeitet 2024-05-22T10:33:32.749+0200
1000 Objekt bearb. Wed May 22 10:33:32 CEST 2024
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