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  • 1
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  46. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh), 32. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh), Wissenschaftliche Herbsttagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR); 20180919-20180922; Mannheim; DOCER.26 /20190205/
    Publication Date: 2019-02-06
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 2
    Keywords: EXPRESSION ; Germany ; human ; PATHWAY ; PATHWAYS ; DIAGNOSIS ; screening ; DISEASE ; DISEASES ; MORTALITY ; RISK ; GENE ; GENES ; PATIENT ; NF-KAPPA-B ; ACTIVATION ; kidney ; DONOR ; INDUCTION ; treatment ; TARGET ; STAGE ; IDENTIFICATION ; PROMOTER ; STRESS ; STRESS-RESPONSE ; REGION ; REGIONS ; NF-kappa B ; TARGETS ; FAILURE ; COMPLICATIONS ; BIOPSY ; inflammation ; PROGRAM ; CLUSTER-ANALYSIS ; SIGNATURE ; HLA-A ; PROMOTER REGION ; renal failure ; RISK-FACTOR ; PROGRAMS ; DIABETIC-NEPHROPATHY ; PREVENTS ; CELL-ADHESION MOLECULE-1 ; GLOMERULAR INJURY
    Abstract: Diabetic nephropathy (DN) is the leading cause of end-stage renal failure and a major risk factor for cardiovascular mortality in diabetic patients. To evaluate the multiple pathogenetic factors implicated in DN, unbiased mRNA expression screening of tubulointerstitial compartments of human renal biopsies was combined with hypothesis-driven pathway analysis. Expression fingerprints obtained from biopsies with histological diagnosis of DN (n = 13) and from control subjects (pretransplant kidney donors [n = 71 and minimal change disease [n = 41) allowed us to segregate the biopsies by disease state and stage by the specific expression signatures. Functional categorization showed regulation of genes linked to inflammation in progressive DN. Pathway mapping of nuclear factor-kappa B (NF-kappa B), a master transcriptional switch in inflammation, segregated progressive from mild DN and control subjects by showing upregulation of 54 of 138 known NF-kappa B targets. The promoter regions of regulated NF-kappa B targets were analyzed using Modellnspector, and the NF-kappa B module NFKB_IRFF_01 was found to be specifically enriched in progressive disease. Using this module, the induction of eight NFKB-IRFF-01-dependant genes was correctly predicted in progressive DN (B2M, CCL5/RANTES, CXCL10/IP10, EDN1, HLA-A, HLA-B, IFNB1, and VCAM1). The identification of a specific NF-kappa B promoter module activated in the inflammatory stress response of progressive DN has helped to characterize upstream pathways as potential targets for the treatment of progressive renal diseases such as DN
    Type of Publication: Journal article published
    PubMed ID: 17065335
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  • 3
    Keywords: TRANSPLANTATION ; RECOGNITION ; INTERFERON ; DOUBLE-STRANDED-RNA ; VIRUS-INFECTION ; RIG-I ; TOLL-LIKE RECEPTOR-3 ; 5'-TRIPHOSPHATE RNA ; ANTIVIRAL RESPONSES ; immunology and pathology ; renal tubular epithelial cells ; RENAL-ALLOGRAFTS ; TUBULAR EPITHELIAL-CELLS
    Abstract: Polyomavirus-associated nephropathy (PVAN) is a significant complication after kidney transplantation, often leading to premature graft loss. In order to identify antiviral responses of the renal tubular epithelium, we studied activation of the viral DNA and the double-stranded RNA (dsRNA) sensors Toll-like receptor 3 (TLR3) and retinoic acid inducible gene-I (RIG-I) in allograft biopsy samples of patients with PVAN, and in human collecting duct cells in culture after stimulation by the dsRNA mimic polyriboinosinic:polyribocytidylic acid (poly(I:C)), cytokines, or infection with BK virus. Double staining using immunofluorescence for BK virus and TLR3 showed strong signals in epithelial cells of distal cortical tubules and the collecting duct. In biopsies microdissected to isolate tubulointerstitial lesions, TLR3 but not RIG-I mRNA expression was found to be increased in PVAN. Collecting duct cells in culture expressed TLR3 intracellularly, and activation of TLR3 and RIG-I by poly(I:C) enhanced expression of cytokine, chemokine, and IFN-beta mRNA. This inflammatory response could be specifically blocked by siRNA to TLR3. Finally, infection of the collecting duct cells with BK virus enhanced the expression of cytokines and chemokines. This led to an efficient antiviral immune response with TLR3 and RIG-I upregulation without activation of IL-1beta or components of the inflammasome pathway. Thus, PVAN activation of innate immune defense mechanisms through TLR3 is involved in the antiviral and anti-inflammatory response leading to the expression of proinflammatory cytokines and chemokines.
    Type of Publication: Journal article published
    PubMed ID: 21918500
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  • 4
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  175. Versammlung des Vereins Rheinisch-Westfälischer Augenärzte; 20130201-20130202; Bochum; DOC13rwa22 /20130130/
    Publication Date: 2013-01-31
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 5
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  175. Versammlung des Vereins Rheinisch-Westfälischer Augenärzte; 20130201-20130202; Bochum; DOC13rwa21 /20130130/
    Publication Date: 2013-01-31
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 6
    Keywords: CELLS ; EXPRESSION ; tumor ; CELL ; Germany ; DISEASE ; DISEASES ; POPULATION ; CDNA ; GENE ; GENE-EXPRESSION ; GENES ; PROTEIN ; transcription ; MOLECULES ; PATIENT ; ANTIGEN ; gene expression ; MARKERS ; MUTATIONS ; PARAMETERS ; BENIGN ; EPITHELIAL-CELLS ; RT-PCR ; MANAGEMENT ; FOCAL SEGMENTAL GLOMERULOSCLEROSIS ; GLOMERULAR PROTEIN ; MEMBRANE-PROTEIN ; NEPHRIN ; PATHOPHYSIOLOGY ; PROGRESSIVE NEPHROPATHIES ; RESISTANT NEPHROTIC SYNDROME
    Abstract: For identifying potential diagnostic markers of proteinuric glomerulopathies, glomerular mRNA levels of molecules relevant for podocyte function (alpha-actinin-4, glomerular epithelial protein 1, Wilms tumor antigen 1, synaptopodin, dystroglycan, nephrin, podoplanin, and podocin) were determined by quantitative real-time RT-PCR from microdissected glomeruli. Biopsies from 83 patients with acquired proteinuric diseases were analyzed (minimal change disease [MCD; n = 13], benign nephrosclerosis [n = 16], membranous glomerulopathy [n = 31], focal and segmental glomerulosclerosis [FSGS; n = 9], and controls [n = 14]). Gene expression levels normalized to two different housekeeping transcripts (glyceraldehyde-3-phosphate-dehydrogenase and 18 S rRNA) did not allow a separation between proteinuric disease categories. However, a significant positive correlation between a-actinin-4, glomerular epithelial protein 1, synaptopodin, dystroglycan, Wilms tumor antigen 1, and nephrin was found in all analyzed glomeruli, whereas podocin mRNA expression did not correlate. Because varying amounts of housekeeper cDNA per glomerulus can confound expression ratios relevant for a subpopulation of cells, an "in silico" microdissection was performed using a podocyte-specific cDNA as a reference gene. Expression ratio of podocin to synaptopodin, the two genes with the most disparate expression, allowed a robust separation of FSGS from MCD and nephrosclerosis. Segregation of FSGS from MCD via this ratio was confirmed in an independent population of formaldehyde-fixed archival biopsies (MCD, n = 5; FSGS, n = 4) after glomerular laser capture microdissection. In addition, the expression marker was able to predict steroid responsiveness in diagnostically challenging cases of MCD versus FSGS (n = 6). As the above approach can be performed as an add-on diagnostic tool, these molecular diagnostic parameters could give novel information for the management of proteinuric diseases
    Type of Publication: Journal article published
    PubMed ID: 14569107
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  • 7
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; proliferation ; CELL ; Germany ; human ; DISEASE ; DISEASES ; POPULATION ; GENE-EXPRESSION ; TIME ; PATIENT ; INJURIES ; LIGAND ; MESANGIAL CELLS ; NEPHRITIS ; RESPONSES ; kidney ; MARKER ; renal ; T cell ; T cells ; T-CELL ; T-CELLS ; antibodies ; antibody ; FORM ; TARGET ; NO ; immunohistochemistry ; DIFFERENCE ; NUMBER ; MARKERS ; LYMPHOCYTES ; MIGRATION ; LIGANDS ; RECRUITMENT ; T-LYMPHOCYTES ; T lymphocyte ; TARGETS ; glomerulonephritis ; NEPHROPATHY ; RECEPTORS ; DIFFERENTIAL EXPRESSION ; chemokine ; T lymphocytes ; INJURY ; PROGNOSTIC MARKERS ; targeting ; CHEMOKINE RECEPTOR ; ABSENCE ; COMPARTMENTS ; PATTERN ; CCR5 ; TRANSPLANT REJECTION ; CD3 ; REAL-TIME ; mRNA ; GLOMERULAR-DISEASES ; RENAL BIOPSIES ; CHEMOKINE RECEPTORS ; CHEMOKINE RECEPTOR CXCR3 ; chemokines ; HUMAN KIDNEY-DISEASES ; INDUCIBLE PROTEIN-10 ; lupus ; LYMPHOCYTE-FIBROBLAST INTERACTIONS ; MESANGIAL CELL ; PROLIFERATIVE GLOMERULONEPHRITIS
    Abstract: Chemokines play pivotal roles in the recruitment of inflammatory cells into the kidney. The chemokine receptors CXCR3 and CCR5 are expressed on activated T lymphocytes, and expression of CXCR3 by mesangial cells has been suggested. Detailed description of CXCR3 expression might form a rational basis for use as a diagnostic marker and for therapeutic CXCR3 targeting in human glomerulonephritis. We studied the expression of CXCR3 in renal biopsies by immunohistochemistry (n = 45), and real time RTPCR (n = 78). Biopsies were from patients with IgA nephropathy, lupus nephritis, and membranoproliferative glomerulonephritis. Furthermore, cultured human mesangial cells (HMC) were studied for CXCR3 expression, and for functional responses to the ligands CXCL10/IP-10 and CXCL9/Mig. CXCR3-positive cells were rarely found in glomerular tufts, but formed a major part of the tubulointerstitial infiltrates. Consistently, CXCR3 mRNA expression was too low to be quantified in glomerular compartments, and was not detectable in HMC. The published staining for CXCR3 of mesangial cells could be traced to cross-reactivity of an antibody for CXCR3 with a potentially related chemokine receptor as revealed by FACS analysis. Despite an absence of CXCR3 expression, mesangial cells reacted to CXCR3 ligands by proliferation and migration, which was blocked by pertussis toxin but not by an anti-CXCR3 antibody. These results indicate that HMC do not express the classical CXCR3, but may potentially express a related receptor with shared ligand specificity. By immunohistochemistry the number of CXCR3-positive cells, mainly interstitial T cells, correlated with renal function, proteinuria, and percentage of globally sclerosed glomeruli. A significant morphological and numerical correlation between CD3, CXCR3, and CCR5-positive cells indicated a CXCR3/CCR5 double-positive T cell population. No apparent difference in the CXCR3 expression pattern was found between disease entities. CXCR3 expression was localized to interstitial T cells, and these cells correlated strongly with important prognostic markers. Therefore interstitial CXCR3, as well as CCR5-positive T cells might play an important role during progressive loss of renal function, and are potential therapeutic targets in human glomerular diseases
    Type of Publication: Journal article published
    PubMed ID: 14742268
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  • 8
    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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  • 9
    Keywords: EXPRESSION ; Germany ; MICROSCOPY ; DIAGNOSIS ; RNA ; TISSUE ; PATIENT ; NEPHRITIS ; DNA ; kidney ; TISSUES ; ANTIGEN ; ACID ; virus ; immunohistochemistry ; REPLICATION ; GENE-EXPRESSION ANALYSIS ; MANAGEMENT ; LIGHT ; RECIPIENTS ; VIRAL LOAD ; polymerase chain reaction ; TRANSPLANT RECIPIENTS ; POLYOMAVIRUS ; JC virus ; complication ; CIDOFOVIR ; native kidney ; BK virus ; SV40 T-antigen ; URINE CYTOLOGY ; VIRUS-ASSOCIATED NEPHROPATHY
    Abstract: Polyomavirus mediated nephropathy is an increasingly recognized complication in renal transplant recipients. In all, 362 renal biopsies collected from 15 European transplant centers were analyzed for presence of Polyomavirus nucleic acid (BK virus [BKV] and JC virus [JCV]). We evaluated 302 biopsies of patients with renal allograft dysfunction, including three with known BKV allograft nephropathy (BKVAN), and 60 native kidney biopsies. BKV DNA was detected in 8 of the 302 (2.6 %) biopsies obtained for transplant dysfunction, but in none of the controls. BKV RNA, indicating active viral replication, was found in all BKV DNA positive biopsies available for mRNA expression studies. Retrospective immunohistochemical staining was positive for SV40 large T antigen in all seven evaluated biopsies. BKV DNA and RNA were detected in biopsy tissues from patients with inconspicuous light microscopy for BKVAN. Further studies will evaluate the potential of intrarenal viral BKV RNA as an early predictor for BKVAN
    Type of Publication: Journal article published
    PubMed ID: 16177632
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  • 10
    Keywords: Germany ; DIAGNOSIS ; COHORT ; PATIENT ; INFECTION ; kidney ; virus ; immunohistochemistry ; PCR ; Jun ; STEM-CELL TRANSPLANTATION ; BONE-MARROW TRANSPLANTATION ; MANAGEMENT ; RENAL-FAILURE ; SIMIAN-VIRUS-40 ; TRANSPLANT RECIPIENTS ; complication ; cardiac transplantation ; CIDOFOVIR ; HEMORRHAGIC CYSTITIS ; INTERSTITIAL NEPHRITIS ; native kidney ; polyoma virus ; POLYOMAVIRUS NEPHROPATHY ; renal failure
    Abstract: Polyomavirus-mediated nephropathy is an increasingly recognized complication in renal transplant recipients, but data on the status of viral activity in the native kidneys of non-renal solid organ recipients are limited. Thirteen native kidney biopsies of heart transplant recipients with significant renal impairment were evaluated for the evidence of polyomavirus reactivation by immunohistochemistry and PCR. One case of BK virus-mediated nephropathy in a cardiac transplant recipient exposed to high levels of immunosuppressive drugs was identified. Clinical and histopathological findings of this patient progressing to terminal renal failure are discussed in detail. In conclusion, polyomavirus reactivation in native kidneys of heart transplant recipients can cause significant renal impairment and should be considered in the differential diagnosis in this patient cohort
    Type of Publication: Journal article published
    PubMed ID: 15888070
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