ArticleThe American journal of pathology2006
Increased expression of integrin alphavbeta5 induces the myofibroblastic differentiation of dermal fibroblasts.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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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
96 citing papers in PubMed, 171 citations in OpenAlex.
- Article
- Distinct Roles of Surface Nanostructure and Polymer Degradation in Fibroblast Response to Device Design.Research square · 2025Article
- Distinct Roles of Surface Nanostructure and Polymer Degradation in Fibroblast Response to Device Design.bioRxiv : the preprint server for biology · 2025Article
- Review
- Novel transcripts of EMT driving the malignant transformation of oral submucous fibrosis.Scientific reports · 2025Article
- MiR-122 promotes metastasis of hepatoma cells by modulating RBM47-integrin alpha V-TGF-beta signaling.PloS one · 2025Article
- Salirasib Inhibits the Expression of Genes Involved in Fibrosis in Fibroblasts of Systemic Sclerosis Patients.Immunity, inflammation and disease · 2024Article
- A two-way street - cellular metabolism and myofibroblast contraction.NPJ Regenerative medicine · 2024Review
- Cellular cross-talk drives mesenchymal transdifferentiation in diabetic kidney disease.Frontiers in medicine · 2024Review
- Integrins as a bridge between bacteria and cells: key targets for therapeutic wound healing.Burns & trauma · 2024Review
- The formin DAAM1 regulates the deubiquitinase activity of USP10 and integrin homeostasis.European journal of cell biology · 2023Article
- Back to the future: targeting the extracellular matrix to treat systemic sclerosis.Nature reviews. Rheumatology · 2023Review
- Dupuytren's Disease Is Mediated by Insufficient TGF-β1 Release and Degradation.International journal of molecular sciences · 2023Article
- Extracellular matrix-induced signaling pathways in mesenchymal stem/stromal cells.Cell communication and signaling : CCS · 2023Review
- Cell Adhesion Molecules in Fibrotic Diseases.Biomedicines · 2023Review
- The Role of Myofibroblasts in Physiological and Pathological Tissue Repair.Cold Spring Harbor perspectives in biology · 2023Review
- Role of integrins in the development of fibrosis in the trabecular meshwork.Frontiers in ophthalmology · 2023Review
- Extracellular matrix stiffness-The central cue for skin fibrosis.Frontiers in molecular biosciences · 2023Review
- Canadian Contributions in Fibroblast Biology.Cells · 2022Review
- Spatiotemporal control of myofibroblast activation in acoustically-responsive scaffolds via ultrasound-induced matrix stiffening.Acta biomaterialia · 2022Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The biological effect of cytokines is mainly determined by the cytokine-receptor interaction, which is modulated by the concentration and the activity of cytokines and/or their receptors. Because alphav-containing integrins can bind to and/or activate latent TGF-beta, these integrins have been thought to be involved in the pathogenesis of fibrotic disorders. Our recent observations that alphavbeta5 is up-regulated in scleroderma fibroblasts and that the transient overexpression of alphavbeta5 increases the human alpha2(I) collagen gene expression in normal fibroblasts suggest the involvement of alphavbeta5 in the self-activation system in scleroderma fibroblasts. In this study, we established stable transfectants with alphavbeta5 using normal dermal fibroblasts and demonstrated that such cells differentiated into myofibroblasts by the stimulation of autocrine TGF-beta. This observation is explained by 1) alphavbeta5 recruiting latent TGF-beta1 on the cell surface, 2) endogenous active TGF-beta localizing on the cell surface, and 3) alphavbeta5 interacting with TGF-beta receptors. Furthermore, blockade of alphavbeta5 reversed the myofibroblastic phenotype in scleroderma fibroblasts. These data identify a novel mechanism for the establishment of autocrine TGF-beta signaling in dermal fibroblasts by the up-regulation of alphavbeta5 and suggest the possibility of regulating fibrotic disorders, especially scleroderma, by targeting this integrin.
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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.