Urokinase type plasminogen activator mediates Interleukin-17-induced peripheral blood mesenchymal stem cell motility and transendothelial migration
| Autor: | Aleksandra Jauković, Jelena Krstic, Slavko Mojsilović, Diana Bugarski, Vesna Ilić, Juan F. Santibanez, Drenka Trivanović, Hristina Obradović, Ivana Okić-Đorđević, Tamara Kukolj |
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| Rok vydání: | 2015 |
| Předmět: |
Motility
Peripheral blood mesenchymal stem cells Matrix metalloproteinase Cell Line Immunophenotyping Proinflammatory cytokine Mice Cell Movement Cell Adhesion medicine Animals Humans Urokinase type plasminogen activator Extracellular Signal-Regulated MAP Kinases Molecular Biology Migration Transendothelial migration Urokinase Blood Cells Receptors Interleukin-17 biology Interleukin-17 Mesenchymal stem cell Transendothelial and Transepithelial Migration Cell Polarity Endothelial Cells Mesenchymal Stem Cells Cell Biology Urokinase-Type Plasminogen Activator Matrix Metalloproteinases Fibronectins Cell biology Urokinase receptor Fibronectin biology.protein Collagen Plasminogen activator medicine.drug |
| Zdroj: | Biochimica et Biophysica Acta-Molecular Cell Research |
| ISSN: | 0167-4889 |
| DOI: | 10.1016/j.bbamcr.2014.11.025 |
| Popis: | Mesenchymal stem cells (MSCs) have the potential to migrate toward damaged tissues increasing tissue regeneration. Interleukin-17 (IL-17) is a proinflammatory cytokine with pleiotropic effects associated with many inflammatory diseases. Although IL-17 can modulate MSC functions, its capacity to regulate MSC migration is not well elucidated so far. Here, we studied the role of IL-17 on peripheral blood (PB) derived MSC migration and transmigration across endothelial cells. IL-17 increased PB-MSC migration in a wound healing assay as well as cell mobilization from collagen gel. Concomitantly IL-17 induced the expression of urokinase type plasminogen activator (uPA) without affecting matrix metalloproteinase expression. The incremented uPA expression mediated the capacity of IL-17 to enhance PB-MSC migration in a ERK1,2 MAPK dependent way. Also, IL-17 induced PB-MSC migration alongside with changes in cell polarization and uPA localization in cell protrusions. Moreover, IL-17 increased PB-MSC adhesion to endothelial cells and transendothelial migration, as well as increased the capacity of PB-MSC adhesion to fibronectin, in an uPA-dependent fashion. Therefore, our data suggested that IL-17 may act as chemotropic factor for PB-MSCs by incrementing cell motility and uPA expression during inflammation development. |
| Databáze: | OpenAIRE |
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