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Abstract: TH-PO823

Circulating Autoantibodies in Lupus Nephritis Patients Target the Cytoskeleton Linking Protein, Moesin, and Disrupt Podocyte Actin Cytoskeleton

Session Information

Category: Glomerular Diseases

  • 1202 Glomerular Diseases: Immunology and Inflammation


  • Caster, Dawn J., University of Louisville, Louisville, Kentucky, United States
  • Korte, Erik, University of Louisville, Louisville, Kentucky, United States
  • Merchant, Michael, University of Louisville Medicine, Louisville, Kentucky, United States
  • Klein, Jon B., University of Louisville Kidney Disease Program, Louisville, Kentucky, United States
  • Tandon, Shweta, University of Louisville, Louisville, Kentucky, United States
  • McLeish, Kenneth R., University of Louisville, Louisville, Kentucky, United States
  • Powell, David W., University of Louisville, Louisville, Kentucky, United States

The pathogenesis of lupus nephritis (LN) is characterized by glomerular deposition of immune complexes (IC) containing nucleosomes and anti-nuclear autoantibodies. However, proteomic studies in LN and other glomerular diseases identified a number of autoantibodies against tissue proteins. We used a targeted proteomic approach combining immunoblot analysis of human podocyte membrane proteins using sera from LN patients with high performance MS to identify moesin as a candidate target protein. We showed that autoantibodies against moesin were present in the sera of patients with proliferative LN and glomeruli in renal biopsies from those patients showed increased expression of moesin. This study tested the hypothesis that autoantibodies to moesin participated in IC formation in LN.


Frozen remnant kidney biopsy samples from patients with proliferative LN were cut into 4-6 µm sections (n= 5) and incubated with anti-moesin antibody at 1:50 overnight followed by sequential incubation with: 1) fluorescent secondary antibody at 1:200 2) fluorescent conjugated anti-human IgG at 1:200. Images were obtained on confocal microscopy. A human-derived podocyte cell line was cultured on collagen-coated glass bottom dishes at 37°C for 8-10 days. Cells were serum starved with 0.5% FBS medium 24 h before anti-moesin antibody, IgG controls, or vehicle was added for 24 h. Actin organization was detected by staining with rhodamine-phalloidin for 30 minutes. Rhodamine staining on confocal microscopy images was analyzed visually and for actin anisotropy by FibrilTool.


To determine if moesin was contained in IC, renal biopsies from patients with proliferative LN were examined for co-localization of moesin and IgG. Confocal images showed minimal co-localization, indicating anti-moesin autoantibodies were not participating in IC formation. As moesin is a cytoskeletal linking protein, the ability of anti-moesin to disrupt podocyte actin organization was tested. Podocytes cultivated with anti-moesin antibodies, but not control IgG or vehicle, showed loss of actin cytoskeletal organization and decreased anisotropy.


We conclude that autoantibodies against moesin may participate in glomerular injury in LN by disruption of podocyte cytoskeletal organization.


  • NIDDK Support