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Article: Monocyte-and endothelial-derived microparticles induce an inflammatory phenotype in human podocytes

TitleMonocyte-and endothelial-derived microparticles induce an inflammatory phenotype in human podocytes
Authors
Issue Date2011
Citation
Nephron - Experimental Nephrology, 2011, v. 119 n. 3, p. e58-e66 How to Cite?
AbstractBackground/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 Identifierhttp://hdl.handle.net/10722/195501
ISSN
2015 Impact Factor: 1.531
2015 SCImago Journal Rankings: 1.030
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorEyre, J-
dc.contributor.authorBurton, JO-
dc.contributor.authorSaleem, MA-
dc.contributor.authorMathieson, PW-
dc.contributor.authorTopham, PS-
dc.contributor.authorBrunskill, NJ-
dc.date.accessioned2014-02-28T06:12:14Z-
dc.date.available2014-02-28T06:12:14Z-
dc.date.issued2011-
dc.identifier.citationNephron - Experimental Nephrology, 2011, v. 119 n. 3, p. e58-e66-
dc.identifier.issn1660-2129-
dc.identifier.urihttp://hdl.handle.net/10722/195501-
dc.description.abstractBackground/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.languageeng-
dc.relation.ispartofNephron - Experimental Nephrology-
dc.titleMonocyte-and endothelial-derived microparticles induce an inflammatory phenotype in human podocytes-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1159/000329575-
dc.identifier.scopuseid_2-s2.0-80051621508-
dc.identifier.volume119-
dc.identifier.issue3-
dc.identifier.spagee58-
dc.identifier.epagee66-
dc.identifier.isiWOS:000296751000002-

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