ArticlePloS one2012
Degradation of internalized αvβ5 integrin is controlled by uPAR bound uPA: effect on β1 integrin activity and α-SMA stress fiber assembly.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- A Novel Insight into Chronic Pancreatitis Pathogenesis: the USP1/ITGB5 Axis-Mediated Stellate Cell Activation.Inflammation · 2026Article
- uPAR deficiency triggers TGFβ1-mediated fibrotic remodeling in a cardiac perivascular-like microenvironment.Stem cell research & therapy · 2026Article
- 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
- USP10 Promotes Fibronectin Recycling, Secretion, and Organization.Investigative ophthalmology & visual science · 2021Article
- Palladin isoforms 3 and 4 regulate cancer-associated fibroblast pro-tumor functions in pancreatic ductal adenocarcinoma.Scientific reports · 2021Article
- USP10 Targeted Self-Deliverable siRNA to Prevent Scarring in the Cornea.Molecular therapy. Nucleic acids · 2020Article
- Cardiac phenotype in mouse models of systemic autoimmunity.Disease models & mechanisms · 2019Review
- The deubiquitylase USP10 regulates integrin β1 and β5 and fibrotic wound healing.Journal of cell science · 2017Article
- Matrix-regulated integrin αeLife · 2017Article
- Integrins in Wound Healing.Advances in wound care · 2014Review
- Urokinase plasminogen activator gene deficiency inhibits fracture cartilage remodeling.Journal of bone and mineral metabolism · 2014Article
- A novel cell adhesion region in tropoelastin mediates attachment to integrin αVβ5.The Journal of biological chemistry · 2014Article
- Mutations in PDGFRB cause autosomal-dominant infantile myofibromatosis.American journal of human genetics · 2013Article
- Reversal of myofibroblast differentiation by prostaglandin E(2).American journal of respiratory cell and molecular biology · 2013Article
- Clinical significance of integrin αvβ6 expression effects on gastric carcinoma invasiveness and progression via cancer-associated fibroblasts.Medical oncology (Northwood, London, England) · 2013Article
- uPA binding to PAI-1 induces corneal myofibroblast differentiation on vitronectin.Investigative ophthalmology & visual science · 2012Article
- The tumor suppressor gene ARHI (DIRAS3) inhibits ovarian cancer cell migration through multiple mechanisms.Cell adhesion & migrationArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Myofibroblasts (Mfs) that persist in a healing wound promote extracellular matrix (ECM) accumulation and excessive tissue contraction. Increased levels of integrin αvβ5 promote the Mf phenotype and other fibrotic markers. Previously we reported that maintaining uPA (urokinase plasminogen activator) bound to its cell-surface receptor, uPAR prevented TGFβ-induced Mf differentiation. We now demonstrate that uPA/uPAR controls integrin β5 protein levels and in turn, the Mf phenotype. When cell-surface uPA was increased, integrin β5 levels were reduced (61%). In contrast, when uPA/uPAR was silenced, integrin β5 total and cell-surface levels were increased (2-4 fold). Integrin β5 accumulation resulted from a significant decrease in β5 ubiquitination leading to a decrease in the degradation rate of internalized β5. uPA-silencing also induced α-SMA stress fiber organization in cells that were seeded on collagen, increased cell area (1.7 fold), and increased integrin β1 binding to the collagen matrix, with reduced activation of β1. Elevated cell-surface integrin β5 was necessary for these changes after uPA-silencing since blocking αvβ5 function reversed these effects. Our data support a novel mechanism by which downregulation of uPA/uPAR results in increased integrin αvβ5 cell-surface protein levels that regulate the activity of β1 integrins, promoting characteristics of the persistent Mf.
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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.