ArticleThe American journal of pathology2004
Increased expression levels of integrin alphavbeta5 on scleroderma fibroblasts.
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 27 papers.
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Who cites it
27 citing papers in PubMed, 78 citations in OpenAlex.
- Transforming growth factor β latency: A mechanism of cytokine storage and signalling regulation in liver homeostasis and disease.JHEP reports : innovation in hepatology · 2022Review
- The Pathogenesis of Systemic Sclerosis: An Understanding Based on a Common Pathologic Cascade across Multiple Organs and Additional Organ-Specific Pathologies.Journal of clinical medicine · 2020Review
- Current and Potential New Targets in Systemic Sclerosis Therapy: a New Hope.Current rheumatology reports · 2020Review
- DZ2002 ameliorates fibrosis, inflammation, and vasculopathy in experimental systemic sclerosis models.Arthritis research & therapy · 2019Article
- Ongoing clinical trials and treatment options for patients with systemic sclerosis-associated interstitial lung disease.Rheumatology (Oxford, England) · 2019Review
- Identification of regulators of the myofibroblast phenotype of primary dermal fibroblasts from early diffuse systemic sclerosis patients.Scientific reports · 2019Article
- Recent advances in the treatment of skin involvement in systemic sclerosis.Inflammation and regeneration · 2017Review
- αv integrins: key regulators of tissue fibrosis.Cell and tissue research · 2016Review
- Epigenetics and systemic sclerosis.Seminars in immunopathology · 2015Review
- Genome-wide DNA methylation analysis in dermal fibroblasts from patients with diffuse and limited systemic sclerosis reveals common and subset-specific DNA methylation aberrancies.Annals of the rheumatic diseases · 2015Article
- Endothelin receptor blockade ameliorates vascular fragility in endothelial cell-specific Fli-1-knockout mice by increasing Fli-1 DNA binding ability.Arthritis & rheumatology (Hoboken, N.J.) · 2015Article
- Fibrosis, vascular activation, and immune abnormalities resembling systemic sclerosis in bleomycin-treated Fli-1-haploinsufficient mice.Arthritis & rheumatology (Hoboken, N.J.) · 2015Article
- Bosentan reverses the pro-fibrotic phenotype of systemic sclerosis dermal fibroblasts via increasing DNA binding ability of transcription factor Fli1.Arthritis research & therapy · 2014Article
- A novel cell adhesion region in tropoelastin mediates attachment to integrin αVβ5.The Journal of biological chemistry · 2014Article
- Integrin-mediated regulation of TGFβ in fibrosis.Biochimica et biophysica acta · 2013Review
- Molecular and cellular mechanisms of pulmonary fibrosis.Fibrogenesis & tissue repair · 2012Article
- Understanding fibrosis in systemic sclerosis: shifting paradigms, emerging opportunities.Nature reviews. Rheumatology · 2011Review
- Amelioration of dermal fibrosis by genetic deletion or pharmacologic antagonism of lysophosphatidic acid receptor 1 in a mouse model of scleroderma.Arthritis and rheumatism · 2011Article
- The lens as a model for fibrotic disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2011Review
- Fibrosis in systemic sclerosis: emerging concepts and implications for targeted therapy.Autoimmunity reviews · 2011Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Integrin alphavbeta5 is a receptor for vitronectin, a plasma glycoprotein that is also distributed in extracellular matrix of various tissues. Matrix-bound vitronectin has the potential to stabilize the active form of plasminogen activator inhibitor-1, resulting in the inhibition of the plasmin-mediated pericellular proteolytic cascade. In this study, we compared the levels of alphavbeta5 and matrix-bound vitronectin between normal and scleroderma fibroblasts and investigated the association with fibrosis. We demonstrated that alphavbeta5 was up-regulated on scleroderma fibroblasts. The up-regulated alphavbeta5 contributed to the increase in vitronectin-binding ability in scleroderma fibroblasts, which led to the vitronectin-dependent activation of plasminogen activator inhibitor-1. In immunohistochemistry, the alphav and beta5 subunits were stained strongly on scleroderma fibroblasts and the amount of vitronectin was increased in the pericellular matrix of those cells. The transient overexpression of alphavbeta5 on normal fibroblasts enhanced the human alpha2(I) collagen promoter activity through Sp-1 and Smad3 as well as the vitronectin-dependent plasminogen activator inhibitor-1 activity. This effect on the promoter activity was also observed in the absence of vitronectin and completely disappeared in the presence of anti-alphavbeta5 antibody. These results indicate that the up-regulated alphavbeta5 may contribute to the phenotypical alteration of scleroderma fibroblasts, while at the same time suppressing the plasmin-mediated pericellular proteolytic cascade.
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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 Socratic graph.