Nephritogenic Anti‐DNA antibodies regulate gene expression in MRL/<i>lpr</i> mouse glomerular mesangial cells

Qing, Xiaoping; Zavadil, Jiří; Crosby, Meredith E.; Hogarth, P. Mark; Hahn, Bevra H.; Mohan, Chandra; Gilkeson, Gary S.; Böttinger, Erwin P.; Putterman, Chaim

doi:10.1002/art.21934

Cited by 72 publications

(81 citation statements)

References 42 publications

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“…Moreover, urinary lipocalin-2 levels were increased in the mice up to 9 weeks after disease induction, coinciding with the presence of florid crescent formation. These results, together with our previous (9) and current data and the published evidence on an association between pediatric lupus nephritis and lipocalin-2 up-regulation (20), strongly support our assertion that urinary lipocalin-2 is a promising potential marker of renal involvement in SLE. As mentioned above, previous studies have indicated that other forms of renal injury, including ischemia, nephrotoxic drugs, or infection, can also up-regulate lipocalin-2 expression in the kidneys (14)(15)(16)(17)(18)(19).…”

Section: Discussionsupporting

confidence: 90%

“…Pathogenic anti-dsDNA monoclonal antibodies up-regulate the expression of lipocalin-2 in glomerular mesangial cells in vitro and also in the kidneys when administered in vivo (9). In the present cross-sectional study, we showed that urinary lipocalin-2 was significantly higher in lupus patients with active nephritis than in those without nephritis.…”

Section: Discussionsupporting

confidence: 51%

“…We recently reported that in vitro treatment targeting kidney mesangial cells with pathogenic murine anti-dsDNA monoclonal antibodies, but not nonpathogenic control antibodies, modulated the expression of inflammatory genes relevant to the pathogenesis of nephritis (9). One of the most dramatically overexpressed genes was lipocalin-2, also known as neutrophil gelatinase-associated lipocalin, or NGAL.…”

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confidence: 99%

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Urinary lipocalin‐2 is associated with renal disease activity in human lupus nephritis

Pitashny¹,

Schwartz²,

Qing³

et al. 2007

Arthritis & Rheumatism

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122

114

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Objective. Pathogenic monoclonal anti-doublestranded DNA (anti-dsDNA) antibodies up-regulate the expression of lipocalin-2 in glomerular mesangial cells. This study was undertaken to investigate whether polyclonal anti-dsDNA antibodies promote the local secretion of lipocalin-2 in the kidneys of patients with systemic lupus erythematosus (SLE), and whether urinary lipocalin-2 represents a marker of kidney involvement in SLE.Methods. Hispanic, African American, and white patients with SLE and normal healthy control subjects from affiliated hospitals of the Albert Einstein College of Medicine were recruited for this cross-sectional study. Patients were classified based on the presence of active renal disease according to the SLE Disease Activity Index (SLEDAI). Correlations of clinical and laboratory data with urinary and serum levels of lipocalin-2 were assessed.Results. Among SLE patients, urinary lipocalin-2 levels were significantly higher in those with lupus nephritis ( Conclusion. The high prevalence of LN in SLE patients and the prognostic significance of kidney disease support the need for identifying early biomarkers to assess the risk of nephritis development and for following up patients with established disease. These findings indicate that urinary lipocalin-2 is a potential marker of the presence and severity of renal involvement in adult patients with SLE.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 51%

mentioning

confidence: 99%

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Urinary lipocalin‐2 is associated with renal disease activity in human lupus nephritis

Pitashny¹,

Schwartz²,

Qing³

et al. 2007

Arthritis & Rheumatism

Self Cite

122

114

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“…[20][21][22][23][24] These antibodies were found to bind mainly nuclear antigens such as chromatin, histones and dsDNA, and/or components of the glomerular basement membrane. In particular, anti-dsDNA autoantibodies were found to be pathogenic and it has been shown that some anti-dsDNA autoantibodies can by themselves alter the gene expression profile of mesangial cell lines, turning on the expression of inflammatory molecules.…”

Section: Discussionmentioning

confidence: 99%

“…In particular, anti-dsDNA autoantibodies were found to be pathogenic and it has been shown that some anti-dsDNA autoantibodies can by themselves alter the gene expression profile of mesangial cell lines, turning on the expression of inflammatory molecules. 24 Further studies are needed to evaluate whether the absence of antidsDNA autoantibodies in serum from IFNAR À/À (B6.Nba2 Â NZW)F1 mice is accountable for the lack of renal disease development in this model.…”

Section: Discussionmentioning

confidence: 99%

Type I interferon signaling is involved in the spontaneous development of lupus-like disease in B6.Nba2 and (B6.Nba2 × NZW)F1 mice

et al. 2007

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Several studies have described a role for type I interferons (IFNab) in the initiation and/or prolongation of autoimmune diseases. Most pronounced has been the association of disease activity with what is now known as 'the interferon signature' of gene expression in peripheral blood mononuclear cells from lupus patients. In correlation, studies have shown that inhibition of IFNab signaling abrogates disease in various mouse models of lupus. New Zealand black (NZB) and B6.Nba2 congenic mice spontaneously develop elevated levels of serum anti-nuclear autoantibodies (ANAs). Nevertheless, neither of these strains develop fatal renal disease. The female F1 offspring of NZB or B6.Nba2 crossed with New Zealand white (NZW) mice do, however, develop kidney disease. We have previously shown that increases in endogenous IFNab levels in (B6.Nba2 Â NZW)F1 mice leads to accelerated development of renal disease in an IFNab-dependent manner. We now show that B6.Nba2 and (B6.Nba2 Â NZW)F1 mice deficient for the IFNab-receptor fail to develop ANA and renal disease, although the mice have substantial immune complex deposition in the glomeruli. Thus, endogenous IFNab might influence disease by affecting B-cell activation and differentiation, as well as the kidneys' susceptibility to damage, the latter perhaps through induction of a local inflammatory milieu.

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Variability of water uptake studies of biomedical polymers

Valenzuela

Michniak

Kohn

2011

J of Applied Polymer Sci

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We report on two unrelated Brazilian boys with craniofacial anomalies that involve the frontonasal process and the first branchial arch associated with pericallosal lipoma. To our knowledge this condition seems to have been reported only once previously, but may represent a new condition within the group of the frontonasal dysgenesis. Clinical and imaging data, phenotypic evolution, and differential diagnosis are discussed. © 2010 Wiley‐Liss, Inc.

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Nephritogenic Anti‐DNA antibodies regulate gene expression in MRL/lpr mouse glomerular mesangial cells

Cited by 72 publications

References 42 publications

Urinary lipocalin‐2 is associated with renal disease activity in human lupus nephritis

Urinary lipocalin‐2 is associated with renal disease activity in human lupus nephritis

Type I interferon signaling is involved in the spontaneous development of lupus-like disease in B6.Nba2 and (B6.Nba2 × NZW)F1 mice

Variability of water uptake studies of biomedical polymers

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