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10.1038/ki.2014.115 http://scihub22266oqcxt.onion/10.1038/ki.2014.115 24759151!ä!24759151 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24759151&cmd=llinks): Failed to open stream: HTTP request failed! 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Modulation of heparan sulfate in the glomerular endothelial glycocalyx decreases leukocyte influx during experimental glomerulonephritis |pdf=|usr=}}{{24759151}} gab.com Text Modulation of heparan sulfate in the glomerular endothelial glycocalyx decreases leukocyte influx during experimental glomerulonephritis JO: Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=24759151 #FOAvip The glomerular endothelial glycocalyx is postulated to be an important modulator of permeability and inflammation. The glycocalyx consists of complex polysaccharides, the main functional constituent of which, heparan sulfate (HS), is synthesized and modified by multiple enzymes. The N-deacetylase-N-sulfotransferase (Ndst) enzymes initiate and dictate the modification process. Here we evaluated the effects of modulation of HS in the endothelial glycocalyx on albuminuria and glomerular leukocyte influx using mice deficient in endothelial and leukocyte Ndst1 (TEKCre+/Ndst1flox/flox). In these mice, glomerular expression of a specific HS domain was significantly decreased, whereas the expression of other HS domains was normal. In the endothelial glycocalyx, this specific HS structure was not associated with albuminuria or with changes in renal function. However, glomerular leukocyte influx was significantly reduced during antiglomerular basement membrane nephritis, which was associated with less glomerular injury and better renal function. In vitro decreased adhesion of wild-type and Ndst1-deficient granulocytes to Ndst1-silenced glomerular endothelial cells was found, accompanied by a decreased binding of chemokines and L-selectin. Thus, modulation of HS in the glomerular endothelial glycocalyx significantly reduced the inflammatory response in antiglomerular basement membrane nephritis. Twit Text FOAVip Modulation of heparan sulfate in the glomerular endothelial glycocalyx decreases leukocyte influx during experimental glomerulonephritis ????Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=24759151 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24759151 #FOAvip English Wikipedia <ref>{{Cite pmid|24759151}}</ref> Modulation of heparan sulfate in the glomerular endothelial glycocalyx decreases leukocyte influx during experimental glomerulonephritis #MMPMID24759151 Rops AL; Loeven MA; van Gemst JJ; Eversen I; Van Wijk XM; Dijkman HB; van Kuppevelt TH; Berden JH; Rabelink TJ; Esko JD; van der Vlag J Kidney Int 2014[Nov]; 86 (5): 932-42 PMID24759151show ga The glomerular endothelial glycocalyx is postulated to be an important modulator of permeability and inflammation. The glycocalyx consists of complex polysaccharides, the main functional constituent of which, heparan sulfate (HS), is synthesized and modified by multiple enzymes. The N-deacetylase-N-sulfotransferase (Ndst) enzymes initiate and dictate the modification process. Here we evaluated the effects of modulation of HS in the endothelial glycocalyx on albuminuria and glomerular leukocyte influx using mice deficient in endothelial and leukocyte Ndst1 (TEKCre+/Ndst1flox/flox). In these mice, glomerular expression of a specific HS domain was significantly decreased, whereas the expression of other HS domains was normal. In the endothelial glycocalyx, this specific HS structure was not associated with albuminuria or with changes in renal function. However, glomerular leukocyte influx was significantly reduced during antiglomerular basement membrane nephritis, which was associated with less glomerular injury and better renal function. In vitro decreased adhesion of wild-type and Ndst1-deficient granulocytes to Ndst1-silenced glomerular endothelial cells was found, accompanied by a decreased binding of chemokines and L-selectin. Thus, modulation of HS in the glomerular endothelial glycocalyx significantly reduced the inflammatory response in antiglomerular basement membrane nephritis. |*Chemotaxis, Leukocyte[MESH] |Animals[MESH] |Anti-Glomerular Basement Membrane Disease/genetics/immunology/*metabolism/physiopathology/prevention & control[MESH] |Autoantibodies[MESH] |Cell Adhesion[MESH] |Cell Line[MESH] |Chemokines/metabolism[MESH] |Coculture Techniques[MESH] |Disease Models, Animal[MESH] |Down-Regulation[MESH] |Endothelial Cells/immunology/*metabolism[MESH] |Female[MESH] |Glycocalyx/immunology/*metabolism[MESH] |Heparitin Sulfate/*metabolism[MESH] |Kidney Glomerulus/immunology/*metabolism/physiopathology[MESH] |L-Selectin/metabolism[MESH] |Leukocytes/immunology/*metabolism[MESH] |Male[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |RNA Interference[MESH] |Signal Transduction[MESH] |Sulfotransferases/deficiency/genetics[MESH] |Time Factors[MESH]Modulation of heparan sulfate in the glomerular endothelial glycocalyx(epmc).pdf DeepDyve Pubget Overpricing