ArticleThe American journal of pathology2001
Coordinated induction of extracellular proteolysis systems during experimental autoimmune encephalomyelitis in mice.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- The role of TPA I/D and PAI-1 4G/5G polymorphisms in multiple sclerosis.Disease markers · 2014Pooled it
- Roles of the tissue-type plasminogen activator in immune response.Cellular immunology · 2022Review
- An Overview of Peptide-Based Molecules as Potential Drug Candidates for Multiple Sclerosis.Molecules (Basel, Switzerland) · 2021Review
- Blocking PDGF-CC signaling ameliorates multiple sclerosis-like neuroinflammation by inhibiting disruption of the blood-brain barrier.Scientific reports · 2020Article
- Molecular imaging of the urokinase plasminogen activator receptor: opportunities beyond cancer.EJNMMI research · 2020Review
- Fibrotic scar after experimental autoimmune encephalomyelitis inhibits oligodendrocyte differentiation.Neurobiology of disease · 2020Article
- Inflammatory Th17 Cells Express Integrin αvβ3 for Pathogenic Function.Cell reports · 2016Article
- Article
- The Role of TLR4 and Fyn Interaction on Lipopolysaccharide-Stimulated PAI-1 Expression in Astrocytes.Molecular neurobiology · 2015Article
- Article
- The plasminogen activator system: involvement in central nervous system inflammation and a potential site for therapeutic intervention.Journal of neuroinflammation · 2013Article
- Homocysteine has anti-inflammatory properties in a hypercholesterolemic rat model in vivo.Molecular and cellular neurosciences · 2012Article
- Microglia use multiple mechanisms to mediate interactions with vitronectin; non-essential roles for the highly-expressed αvβ3 and αvβ5 integrins.Journal of neuroinflammation · 2011Article
- A dual role for microglia in promoting tissue inhibitor of metalloproteinase (TIMP) expression in glial cells in response to neuroinflammatory stimuli.Journal of neuroinflammation · 2011Article
- Long-term expression of tissue-inhibitor of matrix metalloproteinase-1 in the murine central nervous system does not alter the morphological and behavioral phenotype but alleviates the course of experimental allergic encephalomyelitis.The American journal of pathology · 2010Article
- Article
- Chemokine-like receptor-1 expression by central nervous system-infiltrating leukocytes and involvement in a model of autoimmune demyelinating disease.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- In situ zymography and immunolabeling in fixed and decalcified craniofacial tissues.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2009Article
- Differential transcription of matrix-metalloproteinase genes in primary mouse astrocytes and microglia infected with Theiler's murine encephalomyelitis virus.Journal of neurovirology · 2008Article
- Cleavage of myelin associated glycoprotein by matrix metalloproteinases.Journal of neuroimmunology · 2008Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plasminogen activators (PAs) and matrix metalloproteinases (MMPs) are considered to play an important role in the pathogenesis of multiple sclerosis. Experimental autoimmune encephalomyelitis (EAE) is widely used as an animal model of multiple sclerosis. Whereas several studies have addressed the expression of various MMPs and their inhibitors in the pathogenesis of EAE, the expression of the molecules of the PA system during EAE has not been reported previously. The present study was undertaken to investigate the expression of the molecules of the PA system (tPA, uPA, PAI-1, uPAR, LRP), as well as several members of the MMP family and their inhibitors in the course of actively induced EAE in BALB/c mice. During clinical EAE, the PA system was up-regulated in the central nervous system at several levels. Induction of expression of tPA and PAI-1 transcripts was detected in activated astrocytes in the white matter. Inflammatory cells expressed uPA receptor, uPAR. In situ zymography demonstrated the presence of increased tPA and uPA activities in the areas of the inflammatory damage. Accumulation of fibrin, fibronectin, and vitronectin immunoreactivity was seen in perivascular matrices of symptomatic animals. In addition, transcription of MT1-MMP and metalloelastase (in inflammatory cells), and TIMP-1 (in activated astrocytes) was induced during EAE. Increased gelatinolytic activity was detected at the sites of inflammatory cell accumulation by in situ zymography of fluorescently labeled gelatin; substrate gel zymography identified the up-regulated gelatinolytic activity as gelatinase B. Overall, our study demonstrates concurrent induction of PA and MMP systems during active EAE, supporting further the concept that the neuroinflammatory damage in EAE involves altered balance between multiple extracellular proteases and their inhibitors.
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