ArticleThe American journal of pathology2004
Thy-1 expression regulates the ability of rat lung fibroblasts to activate transforming growth factor-beta in response to fibrogenic stimuli.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
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Who cites it
62 citing papers in PubMed, 118 citations in OpenAlex.
- Characterization of Central and Nasal Orbital Adipose Stem Cells and their Neural Differentiation Footprints.Current stem cell research & therapy · 2024Article
- Fibroblast Activation Protein Alpha (FAPα) in Fibrosis: Beyond a Perspective Marker for Activated Stromal Cells?Biomolecules · 2023Review
- Role and mechanism of CD90Molecular medicine (Cambridge, Mass.) · 2023Review
- Antifibrotic Soluble Thy-1 Correlates with Renal Dysfunction in Chronic Kidney Disease.International journal of molecular sciences · 2023Article
- Thy-1 (CD90)-regulated cell adhesion and migration of mesenchymal cells: insights into adhesomes, mechanical forces, and signaling pathways.Frontiers in cell and developmental biology · 2023Review
- The Role of Mesothelin in Activation of Portal Fibroblasts in Cholestatic Liver Injury.Biology · 2022Review
- Proteomic Analysis Reveals Differential Expression Profiles in Idiopathic Pulmonary Fibrosis Cell Lines.International journal of molecular sciences · 2022Article
- A New Hypothetical Concept in Metabolic Understanding of Cardiac Fibrosis: Glycolysis Combined with TGF-β and KLF5 Signaling.International journal of molecular sciences · 2022Review
- Thy-1-Integrin Interactions inFrontiers in cell and developmental biology · 2022Review
- A robust vasculogenic microfluidic model using human immortalized endothelial cells and Thy1 positive fibroblasts.Biomaterials · 2021Article
- Shotgun Proteomics of Isolated Urinary Extracellular Vesicles for Investigating Respiratory Impedance in Healthy Preschoolers.Molecules (Basel, Switzerland) · 2021Article
- Lack of Thy1 defines a pathogenic fraction of cardiac fibroblasts in heart failure.Biomaterials · 2020Article
- Soluble Thy-1 reverses lung fibrosis via its integrin-binding motif.JCI insight · 2019Article
- Alcohol-Induced Interleukin-17 Expression Causes Murine Lung Fibroblast-to-Myofibroblast Transdifferentiation via Thy-1 Down-Regulation.Alcoholism, clinical and experimental research · 2019Article
- Thy-1 in Integrin Mediated Mechanotransduction.Frontiers in cell and developmental biology · 2019Review
- Thy-1 as an Integrator of Diverse Extracellular Signals.Frontiers in cell and developmental biology · 2019Review
- αvβ3 Integrin drives fibroblast contraction and strain stiffening of soft provisional matrix during progressive fibrosis.JCI insight · 2018Article
- Thy-1, a Pathfinder Protein for the Post-genomic Era.Frontiers in cell and developmental biology · 2018Review
- A Profibrotic Phenotype in Naïve and in Fibrotic Lung Myofibroblasts Is Governed by Modulations in Thy-1 Expression and Activation.Mediators of inflammation · 2018Article
- Thy-1 interaction with Fas in lipid rafts regulates fibroblast apoptosis and lung injury resolution.Laboratory investigation; a journal of technical methods and pathology · 2017Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Distinct subpopulations of fibroblasts contribute to lung fibrosis, although the mechanisms underlying fibrogenesis in these subpopulations are not clear. Differential expression of the glycophosphatidylinositol-linked protein Thy-1 affects proliferation and myofibroblast differentiation. Lung fibroblast populations selected on the basis of Thy-1 expression by cell sorting were examined for responses to fibrogenic stimuli. Thy-1 (-) and Thy-1 (+) fibroblast populations were treated with platelet-derived growth factor-BB, interleukin-1beta, interleukin-4, or bleomycin and assessed for activation of transforming growth factor (TGF)-beta, Smad3 phosphorylation, and alpha-smooth muscle actin and fibronectin expression. Thy-1 (-) fibroblasts responded to these stimuli with increased TGF-beta activity, Smad3 phosphorylation, and expression of alpha-smooth muscle actin and fibronectin, whereas Thy-1 (+) fibroblasts resisted stimulation. The unresponsiveness of Thy-1 (+) cells is not because of defective TGF-beta signaling because both subsets respond to exogenous active TGF-beta. Rather, Thy-1 (-) fibroblasts activate latent TGF-beta in response to fibrogenic stimuli, whereas Thy-1 (+) cells fail to do so. Defective activation is common to multiple mechanisms of TGF-beta activation, including thrombospondin 1, matrix metalloproteinase, or plasmin. Thy-1 (-) lung fibroblasts transfected with Thy-1 also become resistant to fibrogenic stimulation, indicating that Thy-1 is a critical biological response modifier that protects against fibrotic progression by controlling TGF-beta activation. These studies provide a molecular basis for understanding the differential roles of fibroblast subpopulations in fibrotic lung disease through control of latent TGF-beta activation.
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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.