ArticleVirulence2018
Fibronectin (FN) cooperated with TLR2/TLR4 receptor to promote innate immune responses of macrophages via binding to integrin β1.
Article in Virulence, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
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- Lineage-specific CK2α deletion reshapes the transcriptome of hematopoietic stem cells toward an immune-primed state.bioRxiv : the preprint server for biology · 2026Article
- TET2 in epigenetic control of immune cells: Implications for inflammatory responses and age-related pathologies.The Journal of biological chemistry · 2026Review
- Fibroblast activation protein (FAP)-mediated promotion of metastasis via the FN1-TGFβ axis and immune suppression in aggressive thyroid cancer.Journal of translational medicine · 2025Article
- Exploring the mechanism of fibronectin extra domain B in the tumor microenvironment and implications for targeted immunotherapy and diagnostics (Review).Molecular medicine reports · 2025Review
- Synoviocyte-chondrocyte triculture model for early-stage PTOA: fibronectin fragment-induced catabolic effectsFrontiers in bioengineering and biotechnology · 2025Article
- Novel proteomics biomarkers of recurrent pregnancy loss reflect the dysregulation of immune interactions at the maternal-fetal interface.Frontiers in immunology · 2025Article
- Granulomatous cellular signatures in nontuberculous and tuberculous mycobacterial infections.Frontiers in microbiology · 2025Article
- ECM remodeling in hypothyroidism-associated MAFLD: mechanisms, clinical relevance, and therapeutic targets.Frontiers in immunology · 2025Review
- Effects of SIPA1L1 on trabecular meshwork extracellular matrix protein accumulation and cellular phagocytosis in POAG.JCI insight · 2024Article
- Landscape of Interactions between Stromal and Myeloid Cells in Ileal Crohn's Disease; Indications of an Important Role for Fibroblast-Derived CCL-2.Biomedicines · 2024Article
- Delivery technologies for therapeutic targeting of fibronectin in autoimmunity and fibrosis applications.Advanced drug delivery reviews · 2024Review
- Mechanoimmunology: Are inflammatory epigenetic states of macrophages tuned by biophysical factors?APL bioengineering · 2022Review
- Recent Progress on the Role of Fibronectin in Tumor Stromal Immunity and Immunotherapy.Current topics in medicinal chemistry · 2022Review
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- Quantitative proteomic analysis reveals the molecular mechanism of the Yesso scallop (Computational and structural biotechnology journal · 2022Article
- Macrophage-extracellular matrix interactions: Perspectives for tissue engineered heart valve remodeling.Frontiers in cardiovascular medicine · 2022Review
- An integrated analysis of mRNAs, lncRNAs, and miRNAs based on weighted gene co-expression network analysis involved in bovine endometritis.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages could adhere to extracellular matrix molecules(ECM) to induce the expression of pro-inflammatory mediators and phagocytosis that contribute to the pathogenesis of pulmonary infection diseases. Fibronectin (FN) is a large glycoprotein capable of interacting with various ECM molecules produced by a variety of cell types and involved in cell attachment and chemotaxis. However, it is unknown whether FN regulates the expression of pro-inflammatory mediators and phagocytosis of macrophages in the injured lung tissue. Here, we investigated the interaction between FN and integrin β1 in macrophages, which promotes toll-like receptor 2/4 (TLR2/TLR4) signaling pathways to enhance expression of pro-inflammatory mediators and phagocytosis by macrophages. Our results show that lipopolysaccharide (LPS), lipoteichoic acid (LTA) and peptidoglycan (PGN) significantly increase FN expression of macrophages; FN substantially enhances interleukin 6 (IL-6), tumor necrosis factor-α (TNFα), ras-related C3 botulinum toxin substrate 1/2 (Rac1/2), and cell division control protein 42 homolog (Cdc42) expression and phagocytosis of macrophages. However, FN could not enhance pro-inflammatory cytokines and phagocytosis of macrophages induced by LPS and PGN in integrin β1-/- macrophages. Furthermore, applied integrin β1 blocking peptide abrogated the effects that FN promotes innate immune responses of macrophages to LPS and PGN. Those data indicated that the enhanced pro-inflammatory mediators and phagocytosis of macrophages by FN-integrin β1 signal was through co-operating with TLR2/TLR4 signaling. This study suggests that FN play an essential role in the pathogenesis of pulmonary infection disease.
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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.