ArticleThe Journal of biological chemistry2010
The first type III repeat in fibronectin activates an inflammatory pathway in dermal fibroblasts.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- Article
- Delivery technologies for therapeutic targeting of fibronectin in autoimmunity and fibrosis applications.Advanced drug delivery reviews · 2024Review
- Extracellular Matrix-Derived Damage-Associated Molecular Patterns (DAMP): Implications in Systemic Sclerosis and Fibrosis.The Journal of investigative dermatology · 2023Review
- Fibronectin in hyperglycaemia and its potential use in the treatment of diabetic foot ulcers: A review.International wound journal · 2023Review
- Induction of pro-inflammatory genes by fibronectin DAMPs in three fibroblast cell lines: Role of TAK1 and MAP kinases.PloS one · 2023Article
- Anastellin impacts on the processing of extracellular matrix fibronectin and stimulates release of cytokines from coronary artery smooth muscle cells.Scientific reports · 2022Article
- Article
- The extracellular matrix as modifier of neuroinflammation and remyelination in multiple sclerosis.Brain : a journal of neurology · 2021Review
- EGFR-Dependent Extracellular Matrix Protein Interactions Might Light a Candle in Cell Behavior of Non-Small Cell Lung Cancer.Frontiers in oncology · 2021Review
- Fibronectin and Its Receptors in Hematopoiesis.Cells · 2020Review
- Role of TLR4 Receptor Complex in the Regulation of the Innate Immune Response by Fibronectin.Cells · 2020Article
- Fibronectin in the Tumor Microenvironment Activates a TLR4-dependent Inflammatory Response in Lung Cancer Cells.Journal of Cancer · 2020Article
- Review
- Endogenous ligands of TLR4 promote unresolving tissue fibrosis: Implications for systemic sclerosis and its targeted therapy.Immunology letters · 2018Review
- Fibronectin (FN) cooperated with TLR2/TLR4 receptor to promote innate immune responses of macrophages via binding to integrin β1.Virulence · 2018Article
- Integrin α4β1 and TLR4 Cooperate to Induce Fibrotic Gene Expression in Response to Fibronectin's EDA Domain.The Journal of investigative dermatology · 2017Article
- TLR4 Ligands Selectively Synergize to Induce Expression of IL-8.Advances in wound care · 2017Article
- Toll-Like Receptor-4 Signaling Drives Persistent Fibroblast Activation and Prevents Fibrosis Resolution in Scleroderma.Advances in wound care · 2017Review
- Inhibition of pro-/active MMP-2 by green tea catechins and prediction of their interaction by molecular docking studies.Molecular and cellular biochemistry · 2017Article
- miR-1207-3p regulates the androgen receptor in prostate cancer via FNDC1/fibronectin.Experimental cell research · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Remodeling of the fibronectin matrix occurs during a variety of pathological and regenerative processes. Cellular generated tensional forces can alter the secondary and tertiary structure of the fibronectin matrix and regulate the exposure of cryptic activities that directly impact cell behavior. In the present study, we evaluated the effect of the partially unfolded Type III fibronectin module, FnIII-1c, on gene expression in dermal fibroblasts. Microarray and PCR analysis indicated that the addition of FnIII-1c to human dermal fibroblasts induced the expression of several inflammatory genes including the cytokines, IL-8 and TNF-α. ELISA analysis indicated that the increased gene expression was accompanied by the secretion of IL-8 and TNF-α protein. FnIII-1c-induced gene expression was preceded by increased phosphorylation of IκB kinase (IKK) and IκBα as well as the nuclear translocation of NFκB. PCR and ELISA analysis showed that inhibition of the NFκB signaling pathway completely blocked the induction of IL-8 and TNF-α. Blocking antibodies to Toll-like receptor 4 inhibited both the activation of the NFκB signaling pathway as well as cytokine expression in response to FnIII-1c. These data suggest that fibronectin matrix remodeling can induce the expression of cytokines by stromal cells present in the tissue microenvironment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.