Nephron Experimental Nephrology
Original Paper
Alterations of Cell Adhesion Molecules in Human Glomerular Endothelial Cells in Response to Nephritis-Associated Plasminogen ReceptorKhan F.a · Yamakami K.b · Mahmood J.a · Li B.a, c · Kikuchi T.a · Kumagai N.a · Morioka T.a · Yoshizawa N.b · Oite T.aaDepartment of Cellular Physiology, Institute of Nephrology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, bDepartment of Public Health, National Defense Medical College, Saitama, Japan; cDepartment of Nephrology, Second Affiliated Hospital, Harbin Medical University, Harbin, PR China
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Article / Publication Details
Published online: December 08, 2006
Issue release date: January 2007
Number of Print Pages: 1
Number of Figures: 10
Number of Tables: 0
eISSN: 1660-2129 (Online)
For additional information: https://www.karger.com/NEE
Abstract
Background: 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. Methods: Expression of cell adhesion molecules were measured by cellular ELISA (enzyme-linked immunosorbent assay), immunofluorescence microscopy and Western blot analysis. Results: 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. Conclusion: 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.
© 2007 S. Karger AG, Basel
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Article / Publication Details
Published online: December 08, 2006
Issue release date: January 2007
Number of Print Pages: 1
Number of Figures: 10
Number of Tables: 0
eISSN: 1660-2129 (Online)
For additional information: https://www.karger.com/NEE
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