Decay-Accelerating Factor Confers Protection Against Complement-Mediated Podocyte Injury in Acute Nephrotoxic Nephritis

Serum Nephritis Glomerular Injury in Acute Nephrotoxic Factor and CD59 in Circumventing Respective Roles of Decay-Accelerating

Statin-induced expression of decay-accelerating factor protects vascular endothelium against complement-mediated injury.

Complement-mediated vascular injury is important in the pathophysiology of atherosclerosis and myocardial infarction. Because recent evidence shows that statins have beneficial effects on endothelial cell (EC) function independent of lipid lowering, we explored the hypothesis that statins modulate vascular EC resistance to complement through the upregulation of complement-inhibitory proteins. H...

AP-1 Transcription Factor JunD Confers Protection from Accelerated Nephrotoxic Nephritis and Control Podocyte-Specific Vegfa Expression

Genetic investigation of crescentic glomerulonephritis (Crgn) susceptibility in the Wistar Kyoto rat, a strain uniquely susceptible to nephrotoxic nephritis (NTN), allowed us to positionally clone the activator protein-1 transcription factor Jund as a susceptibility gene associated with Crgn. To study the influence of Jund deficiency (Jund(-/-)) on immune-mediated renal disease, susceptibility ...

A Role of Polymorphonuclear Leukocytes and Complement in Nephrotoxic Nephritis

In acute nephrotoxic nephritis, polymorphonuclear leukocytes (polymorphs) accumulated in large numbers in the glomeruli in the first 12 hours. The endothelial cells were dislodged by the polymorphs which then came to lie immediately adjacent to the glomerular basement membranes. Ultrastructural changes in neither polymorphs nor basement membranes were observed. Depletion of polymorphs in both r...

The intrinsic complement regulator decay-accelerating factor modulates the biological response to vascular injury.

OBJECTIVE To investigate whether the presence of decay-accelerating factor (or CD55), an intrinsic complement regulator, protects against the development of vascular disease, given that complement activation can affect leukocytes and platelets. METHODS AND RESULTS Leukocyte-platelet complexes are critical for the initiation and progression of atherosclerosis and restenosis; however, the mecha...