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A&R Abstracts – HMGB1

Staff  |  Issue: August 2011  |  August 1, 2011

Conclusion: Increasing the degradation of nucleosomes, reducing their immunogenicity, and preventing binding of nucleosome–IgG complexes in glomeruli together provide an alternative basis for the treatment of lupus nephritis.

 

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Alterations in Wnt pathway activity in mouse serum and kidneys during lupus development. (Arthritis Rheum. 2011;63:513-522.)

Abstract

Objective: The canonical Wnt/β-catenin pathway was recently identified as a factor in the pathogenesis of several renal diseases. The aim of this study was to evaluate Wnt signaling activity during disease development in a murine model of lupus nephritis.

Methods: Wnt activity and Dkk-1 expression were serially assayed in the serum and kidneys of (NZB × NZW)F1 mice during progression of lupus nephritis. The effects of serum obtained from mice with lupus and serum-equivalent concentrations of Dkk-1 on mesangial cells were assessed in vitro.

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Results: Gene expression analyses revealed increased canonical Wnt pathway activity in kidneys during development of lupus nephritis, paralleled by an increase in renal and serum levels of the Wnt inhibitor Dkk-1. Sera obtained from proteinuric-stage (NZB × NZW)F1 mice showed strong Wnt-inhibitory effects in vitro. Dkk-1 concentrations comparable to those observed in lupus-prone mice induced apoptosis in tubular and mesangial cells in vitro, whereas no such effect was seen for the range of concentrations observed in young prediseased mice and control BALB/c mice.

Conclusion: These data demonstrate that renal Wnt signaling activity is increased in lupus and is accompanied by an increase in renal and serum levels of Dkk-1. The Wnt pathway is involved in the turnover of extracellular matrix constituents and represents a potential mediator of the morphologic changes that occur within the glomerulus during the development of nephritis. Furthermore, increased levels of Dkk-1 serve as a potential proapoptotic stimulus in vitro and possibly in vivo and could be an important element in the initiation and progression of systemic and end-organ disease manifestations in systemic lupus erythematosus.

 

The NZM2410-derived lupus susceptibility locus Sle2c1 increases Th17 polarization and induces nephritis in fas-deficient mice. (Arthritis Rheum. 2011;63:764-774.)

Abstract

Objective: Sle2 is a lupus susceptibility locus that has been linked to glomerulonephritis in the NZM2410 mouse. By itself, Sle2 does not induce any autoimmune pathology but results in the accumulation of B-1a cells. This study was designed to assess the contribution of Sle2 to the pathogenesis of autoimmunity.

Methods: Sle2 or its subcongenic intervals (Sle2a, Sle2b, and Sle2c1) were bred to Fas-deficient B6.lpr mice. Lymphoid phenotypes, which were focused on T cells, were assessed by flow cytometry, and histopathologic changes were compared between cohorts of B6.Sle2.lpr congenic mice and B6.lpr mice of ages up to 6 months.

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Filed under:ConditionsResearch RheumSystemic Lupus Erythematosus Tagged with:HMGB1Lupus nephritisResearchSystemic lupus erythematosus

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