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      Induction of Renal Cell Apoptosis by Antibodies and Complement

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          Renal diseases are in many cases associated with the presence of increased numbers of apoptotic cells in the kidney. Apoptosis has been proposed as an important mechanism involved in the resolution of a proliferative response. Furthermore, recent studies indicate its possible involvement in progression of renal disease, leading to sclerosis. Moreover, in an experimental model of acute mesangioproliferative glomerulonephritis in the rat, induced via antibodies directed to Thy-1, evidence was obtained for the occurrence of apoptosis coinciding with the very early induction of mesangial injury. The present review is focused on apoptosis in relation to this model, and discusses recent findings concerning direct involvement of triggering of Thy-1 as well as deposition of terminal complement complexes in the induction of mesangial cell apoptosis.

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          The Cytolytically Inactive Terminal Complement Complex Activates Endothelial Cells to Express Adhesion Molecules and Tissue Factor Procoagulant Activity

          The membrane attack complex of complement (C) in sublytic concentrations stimulates endothelial cells (EC) to express adhesion molecules and to release biologically active products. We have examined the ability of a cytolytically inactive form of this complex, which is incapable of inserting into the cell membrane, to upregulate the expression of adhesion molecules and of tissue factor (TF) procoagulant activity. The inactive terminal C complex (iTCC) was prepared by mixing C5b6, C7, C8, and C9 and was purified by fast protein liquid chromatography on a Superose 12 column. Binding of this complex to EC was found to be dose dependent and was inhibited by anti-C9 antibodies, as assessed both by ELISA using an mAb anti-C9 neoantigen and by measuring cell-bound 125I-labeled iTCC. Exposure of EC to iTCC resulted in a dose- and time-dependent expression of endothelial leukocyte adhesion molecule 1, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 accompanied by increased levels of the corresponding mRNA, but not in the rapid expression of P-selectin. Inactive TCC also induced increased TF activity evaluated by a chromogenic assay that measures the formation of factor Xa. These effects were inhibited by anti-C9 antibodies. The data support the conclusion that iTCC may induce proinflammatory and procoagulant activities on EC.
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            Thy-1-Mediated phosphatidylinositol turnover in cultured rat glomerular mesangial cell


              Author and article information

              Nephron Exp Nephrol
              Cardiorenal Medicine
              S. Karger AG
              April 2001
              11 January 2001
              : 9
              : 2
              : 65-70
              Department of Nephrology, Leiden University Medical Center, Leiden, The Netherlands
              52596 Exp Nephrol 2001;9:65–70
              © 2001 S. Karger AG, Basel

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              Page count
              Figures: 2, References: 25, Pages: 6
              Self URI (application/pdf): https://www.karger.com/Article/Pdf/52596


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