ArticleJournal of cell science2021
Urokinase-type plasminogen activator-mediated crosstalk between N-cadherin and β-catenin promotes wound healing.
Article in Journal of cell science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The trial behind it
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- AP1 Transcription Factor in the Regulation of the Urokinase Plasminogen Activation System.Biomolecules · 2026Review
- Cardiac secreted HSP90α exacerbates pressure overload myocardial hypertrophy and heart failure.Redox biology · 2025Article
- Exploring causal correlations of inflammatory biomarkers in idiopathic normal-pressure hydrocephalus: insights from bidirectional Mendelian randomization analysis.Frontiers in aging neuroscience · 2024Article
- Exploring Co-expression Modules-Traits Correlation through Weighted Gene Co-expression Network Analysis: A Promising Approach in Wound Healing Research.Medical journal of the Islamic Republic of Iran · 2024Article
- Mechanical force drives the initial mesenchymal-epithelial interaction during skin organoid development.Theranostics · 2023Article
- The uPA/uPAR system in astrocytic wound healing.Neural regeneration research · 2022Review
- WNT/β-catenin pathway and circadian rhythms in obsessive-compulsive disorder.Neural regeneration research · 2022Review
- Integrins, cadherins and channels in cartilage mechanotransduction: perspectives for future regeneration strategies.Expert reviews in molecular medicine · 2021Review
- Reactive Astrocytes in Central Nervous System Injury: Subgroup and Potential Therapy.Frontiers in cellular neuroscience · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Urokinase-type plasminogen activator (uPA; encoded by Plau) is a serine proteinase that, in the central nervous system, induces astrocytic activation. β-Catenin is a protein that links the cytoplasmic tail of cadherins to the actin cytoskeleton, thus securing the formation of cadherin-mediated cell adhesion complexes. Disruption of cell-cell contacts leads to the detachment of β-catenin from cadherins, and β-catenin is then degraded by the proteasome following its phosphorylation by GSK3β. Here, we show that astrocytes release uPA following a scratch injury, and that this uPA promotes wound healing via a plasminogen-independent mechanism. We found that uPA induces the detachment of β-catenin from the cytoplasmic tail of N-cadherin (NCAD; also known as CDH2) by triggering its phosphorylation at Tyr654. Surprisingly, this is not followed by degradation of β-catenin because uPA also induces the phosphorylation of the low density lipoprotein receptor-related protein 6 (LRP6) at Ser1490, which then blocks the kinase activity of GSK3β. Our work indicates that the ensuing cytoplasmic accumulation of β-catenin is followed by its nuclear translocation and β-catenin-triggered transcription of the receptor for uPA (Plaur), which in turn is required for uPA to induce astrocytic wound healing.
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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.