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• W2014205093 abstract "<i>Background:</i> Acute post-streptococcal glomerulonephritis (APSGN) is induced by glomerular deposition of nephritogenic streptococcal antigen-antibody complexes. Recently, a streptococcal antigen, nephritis-associated plasminogen receptor (NAPlr) was purified from ruptured streptococcal cell supernatants (RCS). However, the cellular and molecular mechanisms of NAPlr action on the glomerular vas culature are still unknown. <i>Methods:</i> Expression of cell adhesion molecules were measured by cellular ELISA (enzyme-linked immunosorbent assay), immunofluorescence microscopy and Western blot analysis. <i>Results: </i>RCS and NAPlr significantly decreased the PECAM-1 expression in human glomerular endothelial cells (HGECs) as compared to that in the control cells. Plasminogen treatment reversed the RCS or NAPlr-induced decrease of PECAM-1 expression and increase of MCP-1 expression. Immunofluorescent microscopy and Western blot analysis also showed that PECAM-1 expression in HGECs was downregulated upon treatment with RCS or NAPlr and this effect was reversed by plasminogen treatment. Furthermore, we found that tumor necrosis factor-α production in culture medium of HGECs was increased at the lower level when the culture system was treated with RCS. <i>Conclusion:</i> RCS and NAPlr modulated PECAM-1 expression and MCP-1 production in HGECs, indicating the involvement of NAPlr in inflammatory cell accumulation in glomerular tufts and functional abnormality of glomerular microvasculature such as hyperpermeability." @default.
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• W2014205093 date "2006-12-08" @default.
• W2014205093 modified "2023-10-16" @default.
• W2014205093 title "Alterations of Cell Adhesion Molecules in Human Glomerular Endothelial Cells in Response to Nephritis-Associated Plasminogen Receptor" @default.
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• W2014205093 doi "https://doi.org/10.1159/000097840" @default.
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