ArticleThe Journal of clinical investigation1999
Fibronectin fragments modulate monocyte VLA-5 expression and monocyte migration.
Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 57 citations in OpenAlex.
- Redox Control of Integrin-Mediated Hepatic Inflammation in Systemic Autoimmunity.Antioxidants & redox signaling · 2022Review
- Positron Emission Tomography (PET) withMolecular imaging · 2022Article
- Fibrosis after Myocardial Infarction: An Overview on Cellular Processes, Molecular Pathways, Clinical Evaluation and Prognostic Value.Medical sciences (Basel, Switzerland) · 2021Review
- Extracellular Matrix in Ischemic Heart Disease, Part 4/4: JACC Focus Seminar.Journal of the American College of Cardiology · 2020Review
- Changes in cardiac resident fibroblast physiology and phenotype in aging.American journal of physiology. Heart and circulatory physiology · 2018Review
- The extracellular matrix in myocardial injury, repair, and remodeling.The Journal of clinical investigation · 2017Review
- The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis.Circulation research · 2016Review
- Fibronectin Matrix Assembly after Spinal Cord Injury.Journal of neurotrauma · 2015Article
- Using proteomics to uncover extracellular matrix interactions during cardiac remodeling.Proteomics. Clinical applications · 2013Review
- The extracellular matrix modulates fibroblast phenotype and function in the infarcted myocardium.Journal of cardiovascular translational research · 2012Review
- Extracellular matrix roles during cardiac repair.Life sciences · 2010Review
- Monocyte CD49e and 110-120 kDa fibronectin fragments: HIV prognostic indicators independent of viral load and CD4 T-cell counts.AIDS (London, England) · 2009Article
- Targeted deletion or pharmacological inhibition of MMP-2 prevents cardiac rupture after myocardial infarction in mice.The Journal of clinical investigation · 2005Article
- Inflammation and ischemia: macrophages activated by fibronectin fragments enhance the survival of injured cardiac myocytes.Experimental biology and medicine (Maywood, N.J.) · 2004Article
- The extracellular matrix can regulate vascular cell migration, proliferation, and survival: relationships to vascular disease.International journal of experimental pathology · 2000Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
To identify the mechanisms that cause monocyte localization in infarcted myocardium, we studied the impact of ischemia-reperfusion injury on the surface expression and function of the monocyte fibronectin (FN) receptor VLA-5 (alpha(5)beta(1) integrin, CD49e/CD29). Myocardial infarction was associated with the release of FN fragments into cardiac extracellular fluids. Incubating monocytes with postreperfusion cardiac lymph that contained these FN fragments selectively reduced expression of VLA-5, an effect suppressed by specific immunoadsorption of the fragments. Treating monocytes with purified, 120-kDa cell-binding FN fragments (FN120) likewise decreased VLA-5 expression, and did so by inducing a serine proteinase-dependent proteolysis of this beta(1) integrin. We postulated that changes in VLA-5 expression, which were induced by interactions with cell-binding FN fragments, may alter monocyte migration into tissue FN, a prominent component of the cardiac extracellular matrix. Support for this hypothesis came from experiments showing that FN120 treatment significantly reduced both spontaneous and MCP-1-induced monocyte migration on an FN-impregnated collagen matrix. In vivo, it is likely that contact with cell-binding FN fragments also modulates VLA-5/FN adhesive interactions, and this causes monocytes to accumulate at sites where the fragment concentration is sufficient to ensure proteolytic degradation of VLA-5.
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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.