ArticleArteriosclerosis, thrombosis, and vascular biology2017
PAI-1 (Plasminogen Activator Inhibitor-1) Expression Renders Alternatively Activated Human Macrophages Proteolytically Quiescent.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Tissue-Resident Macrophage in Inflammation and Cancer.MedComm · 2026Review
- Mitochondrial ROS drive foam cell formation via STAT5 signaling in atherosclerosis.Science advances · 2025Article
- Phytic acid impairs macrophage inflammatory response in Echinococcus multilocularis infection.Communications biology · 2025Article
- Inflammatory crosstalk impairs phagocytic receptors and aggravates atherosclerosis in clonal hematopoiesis in mice.The Journal of clinical investigation · 2024Article
- Epigenetic and biological age acceleration in children with atopic dermatitis.The journal of allergy and clinical immunology. Global · 2024Article
- Reduced Monocyte and Neutrophil Infiltration and Activation by P-Selectin/CD62P Inhibition Enhances Thrombus Resolution in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Monocyte/macrophage-mediated venous thrombus resolution.Frontiers in immunology · 2024Review
- Pathomechanism of oxidative stress in cardiovascularrenal remodeling and therapeutic strategies.Kidney research and clinical practice · 2022Article
- Review of evidence implicating the plasminogen activator system in blood-brain barrier dysfunction associated with Alzheimer's disease.Ageing and neurodegenerative diseases · 2022Article
- Inhibition of microRNA-494-3p activates Wnt signaling and reduces proinflammatory macrophage polarization in atherosclerosis.Molecular therapy. Nucleic acids · 2021Article
- Systemic and topical administration of spermidine accelerates skin wound healing.Cell communication and signaling : CCS · 2021Article
- Alternative activation of human macrophages enhances tissue factor expression and production of extracellular vesicles.Haematologica · 2021Article
- PI3-kinase inhibition as a strategy to suppress the leukemic stem cell niche in Ph+ chronic myeloid leukemia.American journal of cancer research · 2021Article
- uPAR: An Essential Factor for Tumor Development.Journal of Cancer · 2021Review
- Neutrophil Extracellular Trap Degradation by Differently Polarized Macrophage Subsets.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Protease Activity in Vascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2019Review
- Differential expression of Plg-RBlood · 2019Article
- Siglec-1 Macrophages and the Contribution of IFN to the Development of Autoimmune Congenital Heart Block.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Cardioprotective cytokine interleukin-33 is up-regulated by statins in human cardiac tissue.Journal of cellular and molecular medicine · 2018Article
- Reporting Sex and Sex Differences in Preclinical Studies.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveMacrophages are versatile immune cells capable of polarizing into functional subsets depending on environmental stimulation. In atherosclerotic lesions, proinflammatory polarized macrophages are associated with symptomatic plaques, whereas Th2 (T-helper cell type 2) cytokine-polarized macrophages are inversely related with disease progression. To establish a functional cause for these observations, we analyzed extracellular matrix degradation phenotypes in polarized macrophages. APPROACH AND
resultsWe provide evidence that proinflammatory polarized macrophages rely on membrane-bound proteases including MMP-14 (matrix metalloproteinase-14) and the serine protease uPA (urokinase plasminogen activator) together with its receptor uPAR for extracellular matrix degradation. In contrast, Th2 cytokine alternatively primed macrophages do not show different proteolytic activity in comparison to unpolarized macrophages and lack increased localization of MMP-14 and uPA receptor to the cell membrane. Nonetheless, they express the highest amount of the serine protease uPA. However, uPA activity is blocked by similarly increased expression of its inhibitor PAI-1 (plasminogen activator inhibitor 1). When inhibiting PAI-1 or when analyzing macrophages deficient in PAI-1, Th2 cytokine-polarized macrophages display the same matrix degradation capability as proinflammatory-primed macrophages. Within atherosclerotic lesions, macrophages positive for the alternative activation marker CD206 express high levels of PAI-1. In addition, to test changed tissue remodeling capacities of alternatively activated macrophages, we used a bleomycin lung injury model in mice reconstituted with PAI-1
conclusionsWe were able to demonstrate matrix degradation dependent on membrane-bound proteases in proinflammatory stimulated macrophages and a forced proteolytical quiescence in alternatively polarized macrophages by the expression of PAI-1.
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