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  • DISEASE  (3)
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  • 1
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    Kidney International 64 (6), 1956-1967 
    Keywords: CELLS ; CELL ; Germany ; human ; SYSTEM ; DISEASE ; DISEASES ; PROTEIN ; PROTEINS ; METABOLISM ; EPITHELIA ; NITRIC-OXIDE SYNTHASE ; COMPLEX ; NITRIC-OXIDE ; COMPLEXES ; kidney ; renal ; IONS ; ACID ; ACIDS ; antibodies ; antibody ; NUCLEIC-ACID ; NUCLEIC-ACIDS ; PROGRESSION ; MEMBRANE ; DAMAGE ; GLYCATION END-PRODUCTS ; ATHEROSCLEROSIS ; lipids ; LOW-DENSITY-LIPOPROTEIN ; EPITOPE ; EPITOPES ; ATTENUATION ; glomerulonephritis ; OXYGEN ; COLONY-STIMULATING FACTOR ; URINE ; inflammation ; glomerulonephritis,MPO-hydrogen peroxide-chloride system,renal disease,hypochlorous acid/hypochlorit ; HUMAN ATHEROSCLEROTIC LESIONS ; HUMAN POLYMORPHONUCLEAR LEUKOCYTES ; HYPOCHLORITE-MODIFIED PROTEINS ; ISCHEMIA-REPERFUSION INJURY ; NEUTROPHIL RESPIRATORY BURST ; reactive oxygen species ; RENAL ISCHEMIA/REPERFUSION INJURY ; rodent
    Abstract: In glomerular and tubulointerstitial disease, polymorphonuclear- and monocyte-derived reactive oxygen species may contribute to oxidative modification of proteins, lipids, and nucleic acids. In part, the processes instigated by reactive oxygen species parallel events that lead to the development of atherosclerosis. Myeloperoxidase (MPO), a heme protein and catalyst for (lipo) protein oxidation is present in these mononuclear cells. The ability of MPO to generate hypochlorous acid/hypochlorite (HOCl/OCl-) from hydrogen peroxide in the presence of chloride ions is a unique and defining activity for this enzyme. The MPO-hydrogen peroxide-chloride system leads to a variety of chlorinated protein and lipid adducts that in turn may cause dysfunction of cells in different compartments of the kidney. The aim of this article is to cover and interpret some experimental and clinical aspects in glomerular and tubulointerstitial diseases in which the MPO-hydrogen peroxide-chloride system has been considered an important pathophysiologic factor in the progression but also the attenuation of experimental renal disease. The colocalization of MPO and HOCl-modified proteins in glomerular peripheral basement membranes and podocytes in human membranous glomerulonephritis, the presence of HOCl-modified proteins in mononuclear cells of the interstitium and in damaged human tubular epithelia, the inflammation induced and exacerbated by MPO antibody complexes in necrotizing glomerulonephritis, and the presence of HOCl-modified epitopes in urine following hyperlipidemia-induced renal damage in rodents suggest that MPO is an important pathogenic factor in glomerular and tubulointerstitial diseases. Specifically, the interaction of MPO with nitric oxide metabolism adds to the complexity of actions of oxidants and may help to explain bimodal partly detrimental partly beneficial effects of the MPO-hydrogen peroxide-chloride system in redox-modulated renal diseases
    Type of Publication: Journal article published
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  • 2
    Keywords: CANCER ; EXPRESSION ; Germany ; human ; KINASE ; FOLLOW-UP ; DISEASE ; POPULATION ; DISTINCT ; GENE ; GENE-EXPRESSION ; GENES ; RNA ; SAMPLE ; SAMPLES ; COMPLEX ; COMPLEXES ; kidney ; renal ; score ; IDENTIFICATION ; PROGRESSION ; gene expression ; MARKERS ; PATHOGENESIS ; PARAMETERS ; INTEGRIN ; STRATEGIES ; NEPHROPATHY ; RECEPTORS ; inflammation ; MAPS ; MATRIX ; cDNA array,gene expression,kidney,inflammation,fibrosis,interstitial hydronephrosis,real time RT-PCR ; CHEMOKINE EXPRESSION ; GLOMERULAR-DISEASES ; RENAL BIOPSIES
    Abstract: Background. Gene expression profiling of nephropathies may facilitate development of diagnostic strategies for complex renal diseases as well as provide insight into the molecular pathogenesis of kidney diseases. To test molecular based renal disease categorization, differential gene expression profiles were compared between control and hydronephrotic kidneys showing varying degrees of inflammation and fibrosis.Methods. RNA expression profiles from 9 hydronephrotic and 3 control kidneys were analyzed using small macroarrays dedicated to genes involved in cell-cell contact, matrix turnover, and inflammation. In parallel, the degree of tubulointerstitial inflammation, fibrosis, and tubular atrophy using light microscopy and quantitative immunohistochemical parameters was determined.Results. Hierarchic clustering and self-organizing maps led to a gene expression dendrogram with three distinct nodes representing the control group, four kidneys with high inflammation, and five kidneys giving high fibrosis scores. To evaluate the clinical applicability of the marker set, the expression of nine genes (6Ckine, IL-8, MMP-9, MMP-3, MMP-7, urokinase R, CXCR5, integrin-beta4, and pleiotrophin) was tested in tubulointerstitial samples from routine renal biopsies. Seven mRNA markers showed differential regulation in inflammation and fibrosis in the biopsy population. Clinical follow-up revealed stringent correlation between gene expression data and progression of renal disease, and allowed segregation of the biopsies into progressive or stable disease course based on gene expression profiles.Conclusion. This study suggests the feasibility of gene expression-based disease categorization in human nephropathies based on the extraction of marker gene sets
    Type of Publication: Journal article published
    PubMed ID: 14871410
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  • 3
    Keywords: CELLS ; ENDOTHELIAL-CELLS ; EXPRESSION ; Germany ; DISEASE ; COMPLEX ; NITRIC-OXIDE ; COMPLEXES ; INDUCTION ; RATS ; NECROSIS-FACTOR-ALPHA ; ADHESION MOLECULE-1 ; FAILURE ; reactive oxygen species ; INCREASE ; GENE-TRANSCRIPTION ; MCP-1 ; RISK-FACTOR ; macrophage ; antioxidant enzymes ; LIPOPROTEIN ABNORMALITIES ; VCAM-1
    Abstract: Hyperlipidemia can induce or aggravate renal tubulointerstitial injury. Experiments in a complex rat model with chronic glomerulonephritis and long-standing, coexisting hyperlipidemia suggested that induction of xanthine oxidase (XO), with increased oxygen radical generation, is involved in aggravation of tubulointerstitial injury. To separate the role of XO in the initial events of lipid-mediated tubulointerstitial injury, short-term experiments with diet-induced hyperlipidemia over 21 and 35 days were performed in otherwise healthy rats. XO expression in relation to the antioxidant enzymes was examined in the cortical tubulointerstitium (TIS) and proximal tubules ( PT). Subsequent experiments with XO inhibition were performed, examining tubulointerstitial infiltration with ED1-positive cells and expression of adhesion molecules and monocyte chemoattractant protein-1 (MCP-1) as indicators of early injurious events. Hyperlipidemia increased XO activity in TIS by 40 and 86%, and in PT by 28 and 90% at days 21 and 35, compared with controls on regular diet. This increased activity was associated with increased reactive oxygen species. Among the antioxidant enzymes, glutathione peroxidase activity increased in TIS by 40% and in PT by 90%. Histological evaluation showed a three-fold increase in ED1-positive cells and increased MCP-1 and vascular cell adhesion molecule-1 (VCAM-1) expression at day 35 in the TIS. Inhibition of XO prevented tubulointerstitial ED1 cell infiltration, together with a decreased expression of MCP-1 and VCAM-1. These results point to an important role for XO in the early stage of hyperlipidemia-associated renal injury, mediating macrophage infiltration by a putatively redox-dependent upregulation of MCP-1 and VCAM-1
    Type of Publication: Journal article published
    PubMed ID: 16407880
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