We have recently demonstrated that transformation of mild glomerulonephritis into end-stage kidney disease coincides
with renal DNaseI shut-down in (NZBxNZW)F1 mice and in human lupus nephritis. Down-regulation of DNaseI results
in reduced chromatin fragmentation and deposition of extracellular chromatin complexes in glomerular basement membranes
where they appear in complex with IgG antibodies. Two objectives were regarded central in this study. First, we aimed new
analyses to obtained insight into protection and repair mechanisms in lupus nephritis. The main focus in this study was to resolve
whether inflammation-driving silencing of the renal DNaseI gene expression correlated with increased expression of the anti-
apoptotic and survival protein tumor necrosis factor receptor-associated protein 1 (Trap1). Secondly, we aimed to translate results
from murine lupus nephritis to human lupus nephritis. Mouse and human mRNA expression levels of DNaseI, and Trap1, were
determined and compared with protein expression profiles and clinical data. The data demonstrate that silencing of DNaseI gene
expression is highly negatively correlated with increased sessile expression of the Trap1 gene. Secondly.an acquired reduction in
DNaseI appears to be important for progression of disease in both the murine and human formsof lupus nephritis.The loss of
renal DNaseI seems to initiate a cascade of inflammatory signals leading to the up-regulation of repair proteins like the Trap1.
Ole Petter Rekvig completed his Ph.D.in Medical Immunology in 1981 at the University of Troms?. He has served as professor in molecular immunology and pathology from 1984, and has served as consultant at the University Hospital from 2000. He has published scientific papers on molecular pathology and immunology with a special interest in processes linked to lupus nephritis.
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