ArticlePloS one2013
Urokinase plasminogen activator induces pro-fibrotic/m2 phenotype in murine cardiac macrophages.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- Cellular interactions within the immune microenvironment underpins resistance to cell cycle inhibition in breast cancers.Nature communications · 2025Article
- Macrophage-based therapeutic approaches for cardiovascular diseases.Basic research in cardiology · 2024Review
- Immune cell-mediated venous thrombus resolution.Research and practice in thrombosis and haemostasis · 2023Review
- Human dermal fibroblast-derived exosomes induce macrophage activation in systemic sclerosis.Rheumatology (Oxford, England) · 2023Article
- The uPA/uPAR System Orchestrates the Inflammatory Response, Vascular Homeostasis, and Immune System in Fibrosis Progression.International journal of molecular sciences · 2023Review
- Sex-Specific Differences of the Inflammatory State in Experimental Autoimmune Myocarditis.Frontiers in immunology · 2021Article
- Resolution of Deep Venous Thrombosis: Proposed Immune Paradigms.International journal of molecular sciences · 2020Review
- Fibroblasts and Their Pathological Functions in the Fibrosis of Aortic Valve Sclerosis and Atherosclerosis.Biomolecules · 2019Review
- SerpinB2 inhibits migration and promotes a resolution phase signature in large peritoneal macrophages.Scientific reports · 2019Article
- Plasminogen and the Plasminogen Receptor, Plg-RFrontiers in immunology · 2019Article
- Estramustine Phosphate Inhibits TGF-Analytical cellular pathology (Amsterdam) · 2018Article
- Article
- Global liver gene expression differences in Nelore steers with divergent residual feed intake phenotypes.BMC genomics · 2015Article
- MMP-12 deficiency attenuates angiotensin II-induced vascular injury, M2 macrophage accumulation, and skin and heart fibrosis.PloS one · 2014Article
- Transcriptional changes in bone marrow stromal cells of patients with heart failure.Cell cycle (Georgetown, Tex.) · 2014Article
- Ixmyelocel-T, an expanded multicellular therapy, contains a unique population of M2-like macrophages.Stem cell research & therapy · 2013Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveInflammation and fibrosis are intertwined in multiple disease processes. We have previously found that over-expression of urokinase plasminogen activator in macrophages induces spontaneous macrophage accumulation and fibrosis specific to the heart in mice. Understanding the relationship between inflammation and fibrosis in the heart is critical to developing therapies for diverse myocardial diseases. Therefore, we sought to determine if uPA induces changes in macrophage function that promote cardiac collagen accumulation. METHODS AND
resultsWe analyzed the effect of the uPA transgene on expression of pro-inflammatory (M1) and pro-fibrotic (M2) genes and proteins in hearts and isolated macrophages of uPA overexpressing mice. We found that although there was elevation of the pro-inflammatory cytokine IL-6 in hearts of transgenic mice, IL-6 is not a major effector of uPA induced cardiac fibrosis. However, uPA expressing bone marrow-derived macrophages are polarized to express M2 genes in response to IL-4 stimulation, and these M2 genes are upregulated in uPA expressing macrophages following migration to the heart. In addition, while uPA expressing macrophages express a transcriptional profile that is seen in tumor-associated macrophages, these macrophages promote collagen expression in cardiac but not embryonic fibroblasts.
conclusionsUrokinase plasminogen activator induces an M2/profibrotic phenotype in macrophages that is fully expressed after migration of macrophages into the heart. Understanding the mechanisms by which uPA modulates macrophage function may reveal insights into diverse pathologic processes.
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