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Article: Monocyte-and endothelial-derived microparticles induce an inflammatory phenotype in human podocytes
Title | Monocyte-and endothelial-derived microparticles induce an inflammatory phenotype in human podocytes |
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Authors | |
Keywords | Albumin Glomerular inflammation IL-6 MCP-1 Microparticles Podocyte Proteinuria VEGF |
Issue Date | 2011 |
Citation | Nephron - Experimental Nephrology, 2011, v. 119 n. 3, p. e58-e66 How to Cite? |
Abstract | Background/Aims: Proteinuria is associated with cardiovascular and chronic kidney disease. Microparticles (MPs) are bioactive vesicles shed from activated cells and also linked to cardiovascular disease. MP-like structures have been identified in the glomerular basement membrane, urinary space and between the glomerular basement membrane and the podocyte. We hypothesised that circulating MPs may provide a link between vascular injury and kidney diseases by inducing podocyte phenotypic alterations, thus propagating glomerular dysfunction and proteinuria. Methods:Human umbilical vein endothelial cells and U937 monocytes were stimulated with TNF-α to produce MPs. These MPs were confirmed by electron microscopy, and added to differentiated podocyte monolayers to determine effects on podocyte albumin endocytosis and the production of soluble mediators. Results:Monocyte and endothelial MPs upregulated podocyte production of pro-inflammatory mediators monocyte chemoattractant protein-1 (p < 0.001) and interleukin-6 (p < 0.001). Only monocyte MPs upregulated podocyte secretion of VEGF (p < 0.001), known to regulate glomerular permeability. Endothelial MPs decreased podocyte albumin endocytosis by 13% compared to control cells (p < 0.01). Conclusion:MPs alter endocytic functions of podocytes and induce secretion of pro-inflammatory cytokines, potentially leading to glomerular inflammation in vivo and the development of proteinuria. This study identifies a potential pathophysiological role for circulating MPs in the kidney through effects on the podocyte. © 2011 S. Karger AG, Basel. |
Persistent Identifier | http://hdl.handle.net/10722/195501 |
ISSN | 2016 Impact Factor: 2.238 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Eyre, J | - |
dc.contributor.author | Burton, JO | - |
dc.contributor.author | Saleem, MA | - |
dc.contributor.author | Mathieson, PW | - |
dc.contributor.author | Topham, PS | - |
dc.contributor.author | Brunskill, NJ | - |
dc.date.accessioned | 2014-02-28T06:12:14Z | - |
dc.date.available | 2014-02-28T06:12:14Z | - |
dc.date.issued | 2011 | - |
dc.identifier.citation | Nephron - Experimental Nephrology, 2011, v. 119 n. 3, p. e58-e66 | - |
dc.identifier.issn | 1660-2129 | - |
dc.identifier.uri | http://hdl.handle.net/10722/195501 | - |
dc.description.abstract | Background/Aims: Proteinuria is associated with cardiovascular and chronic kidney disease. Microparticles (MPs) are bioactive vesicles shed from activated cells and also linked to cardiovascular disease. MP-like structures have been identified in the glomerular basement membrane, urinary space and between the glomerular basement membrane and the podocyte. We hypothesised that circulating MPs may provide a link between vascular injury and kidney diseases by inducing podocyte phenotypic alterations, thus propagating glomerular dysfunction and proteinuria. Methods:Human umbilical vein endothelial cells and U937 monocytes were stimulated with TNF-α to produce MPs. These MPs were confirmed by electron microscopy, and added to differentiated podocyte monolayers to determine effects on podocyte albumin endocytosis and the production of soluble mediators. Results:Monocyte and endothelial MPs upregulated podocyte production of pro-inflammatory mediators monocyte chemoattractant protein-1 (p < 0.001) and interleukin-6 (p < 0.001). Only monocyte MPs upregulated podocyte secretion of VEGF (p < 0.001), known to regulate glomerular permeability. Endothelial MPs decreased podocyte albumin endocytosis by 13% compared to control cells (p < 0.01). Conclusion:MPs alter endocytic functions of podocytes and induce secretion of pro-inflammatory cytokines, potentially leading to glomerular inflammation in vivo and the development of proteinuria. This study identifies a potential pathophysiological role for circulating MPs in the kidney through effects on the podocyte. © 2011 S. Karger AG, Basel. | - |
dc.language | eng | - |
dc.relation.ispartof | Nephron - Experimental Nephrology | - |
dc.subject | Albumin | - |
dc.subject | Glomerular inflammation | - |
dc.subject | IL-6 | - |
dc.subject | MCP-1 | - |
dc.subject | Microparticles | - |
dc.subject | Podocyte | - |
dc.subject | Proteinuria | - |
dc.subject | VEGF | - |
dc.title | Monocyte-and endothelial-derived microparticles induce an inflammatory phenotype in human podocytes | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1159/000329575 | - |
dc.identifier.scopus | eid_2-s2.0-80051621508 | - |
dc.identifier.volume | 119 | - |
dc.identifier.issue | 3 | - |
dc.identifier.spage | e58 | - |
dc.identifier.epage | e66 | - |
dc.identifier.isi | WOS:000296751000002 | - |
dc.identifier.issnl | 1660-2129 | - |