Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; IN-VITRO ; proliferation ; IN-VIVO ; MODEL ; DISEASE ; DISTINCT ; MICE ; ACTIVATED MACROPHAGES ; ACTIVATION ; COMPLEX ; CRESCENTIC GLOMERULONEPHRITIS ; INJURIES ; LIGAND ; MESANGIAL CELLS ; MONOCYTE ARREST ; NEPHRITIS ; NITRIC-OXIDE ; RANTES ; RESPONSES
    Abstract: The chemokine CC chemokine ligand (CCL)5/RANTES as well as its respective receptor CCR5 mediate leukocyte infiltration during inflammation and are up-regulated early during the course of glomerulonephritis (GN). We tested the effects of the two CCL5/RANTES blocking analogs, Met-RANTES and amino-oxypentane- RANTES, on the course of horse apoferritin (RAF)induced GN. HAF-injected control mice had proliferative GN with mesangial immune complex deposits of IgG and HAF. Daily i.p. injections of Met-RANTES or amino-oxypentane-RANTES markedly reduced glomerular cell proliferation and glomerular macrophage infiltration, which is usually associated with less glomerular injury and proteinuria in RAF-GN. Surprisingly, however, RAF-GN mice treated with both analogs showed worse disease with mesangiolysis, capillary obstruction, and nephrotic range albuminuria. These findings were associated with an enhancing effect of the CCL5/RANTES analogs on the macrophage activation state, characterized by a distinct morphology and increased inducible NO synthetase expression in vitro and in vivo, but a reduced uptake of apoptotic cells in vivo. The Immoral response and the Th1/Th2 balance in HAF-GN and mesangial cell proliferation in vitro were not affected by the CCL5/RANTES analogs. We conclude that, despite blocking local leukocyte recruitment, chemokine analogs can aggravate some specific disease models, most likely due to interactions with systemic immune reactions, including the removal of apoptotic cells and inducible NO synthetase expression
    Type of Publication: Journal article published
    PubMed ID: 12759447
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; IN-VITRO ; Germany ; human ; DISEASE ; DISEASES ; MICE ; ACTIVATION ; COMPLEX ; MESANGIAL CELLS ; ARTHRITIS ; CELL ACTIVATION ; COMPLEXES ; CUTTING EDGE ; DNA ; IFN-GAMMA ; INFECTION ; kidney ; MACROPHAGES ; MECHANISM ; MESSENGER-RNA ; MESSENGER-RNA EXPRESSION ; MOTIFS ; murine ; OLIGODEOXYNUCLEOTIDES ; RECEPTOR EXPRESSION ; SERA ; TH1 RESPONSES ; TRIGGER
    Abstract: Immune complex glomerulonephritis (GN) often deteriorates during infection with viruses and bacteria that, in contrast to mammals, have DNA that contains many unmethylated CpG motifs. Balb/c mice with horse apoferritin-induced GN (HAF-GN) were treated with either saline, CpG-oligodeoxynucleotides (ODN), or control GpC-ODN. Only CpG-ODN exacerbated HAF-GN with an increase of glomerular macrophages, which was associated with massive albuminuria and increased renal MCP-1/CCL2, RANTES/CCL5, CCR1, CCR2, and CCR5 mRNA expression. CpG-ODN induced a Th1 response as indicated by serum anti-HAF IgG(2a) titers, mesangial IgG(2a) deposits, and splenocyte IFN-gamma secretion. Messenger RNA for the CpG-DNA receptor Toll-like reeptor 9 (TLR9) was present in kidneys with HAF-GN but not in normal kidneys. The source of TLR9 mRNA in HAF-GN could. be infiltrating macrophages or intrinsic renal cells, e.g., mesangial cells; but, in vitro, only murine J774 macrophages expressed TLR9. In J774 cells, CpG-ODN induced the chemokines MCP-1/CCL2 and RANTES/CCL5 and the chemokine receptors CCR1 and CCR5. It is concluded that CpG-DNA can aggravate preexisting GN via a shift toward a Th1 response but also by a novel pathway involving TLR9-mediated chemokine and chemokine receptor expression by macrophages, which may contribute to the enhanced glomerular macrophage recruitment and activation. This mechanism may be relevant during infection-triggered exacerbation of human immune-complex GN and other immune- mediated diseases in general
    Type of Publication: Journal article published
    PubMed ID: 12538732
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
  • 4
    Keywords: MICE ; RESPONSES ; kidney ; PHENOTYPE ; HYPERPLASIA ; HOMEOSTASIS ; aldosterone
    Abstract: Renin expressing cells in the kidney normally appear as mural cells of developing preglomerular vessels and finally impose as granulated juxtaglomerular cells in adult kidneys. The differentiation of renin expressing cells from the metanephric mesenchyme in general, and the potential role of special precursor stages in special, is not well understood. It was the aim of this study therefore to search for renin cell precursors in the kidney. As an experimental model we used kidneys of aldosterone synthase deficient mice which display a prominent compensatory overproduction of renin cells that are arranged in multilayered perivascular cell clusters. We found that the perivascular cell clusters contained two apparently distinct cell types. One staining positive for renin and another one staining positive for type I procollagen (PC1). It appeared as if PC1 and renin expression were inversely related at the cellular level. The proportion of renin positive to PC1 positive cells in the clusters was inversely linked to the rate of salt intake as was overall renin expression. Our findings suggest that the cells in the perivascular cell clusters can reversibly switch between procollagen 1 and renin expression, and that PC1 expressing cells might be precursors of renin cells. Few of those PC1 positive cells were found also in adult wildtype kidneys in the juxtaglomerular lacis cell area, in which renin expression can be induced on demand.
    Type of Publication: Journal article published
    PubMed ID: 23761669
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    Keywords: Germany ; THERAPY ; DIAGNOSIS ; DISEASE ; HISTORY ; PATIENT ; INFECTION ; PATHOGENESIS ; FAILURE ; SERUM ; acute interstitial nephritis ; corticosteroids ; VARIETIES ; ANTIBIOTIC-THERAPY ; acute anuric renal failure ; drug-induced acute interstitial nephritis ; exanthema ; KAWASAKI DISEASE
    Abstract: A 15-year-old girl with a history of Kawasaki disease was admitted to Our nephrological department due to acute renal failure. Despite antibiotic therapy because of fever and the symptoms of a pharyngitis in the last few days, the girl showed persisting fever and developed arthralgias, an exanthema and a rising serum creatinine as well as anuria. A wide variety of differential diagnoses has to be thought of because of the history of the Kawasaki disease (symptoms like fever, pharyingitis, exanthema and arthralgia), i.e. hemolytic-uremic syndrome, vasculitis, ascending infection, postinfection glomerulonephritis. In consideration of etiologically unclear "rapidly progressive renal failure" with anuria and thrombocytopenia an immediate renal biopsy was done and revealed a severe drug induced acute interstitial nephritis. Due to this diagnosis we treated the patient with corticosteroids. Within 4 weeks serum creatinine declined to 1.8 mg/dl but did not normalize
    Type of Publication: Journal article published
    PubMed ID: 16724658
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
    Keywords: RECEPTOR ; APOPTOSIS ; CELLS ; EXPRESSION ; proliferation ; tumor ; Germany ; human ; DISEASE ; GENE-EXPRESSION ; PROTEIN ; RELEASE ; NF-KAPPA-B ; COMPLEX ; CRESCENTIC GLOMERULONEPHRITIS ; MESANGIAL CELLS ; COMPLEXES ; INFECTION ; kidney ; DENDRITIC CELLS ; virus ; LOCALIZATION ; DOUBLE-STRANDED-RNA ; DIFFERENTIAL EXPRESSION ; FACTOR-I ; TOLL-LIKE RECEPTORS ; COLONY-STIMULATING FACTOR ; VIRUS-INFECTION ; LEVEL
    Abstract: Hepatitis C virus (HCV) infection is frequently complicated by glomerulonephritis with immune complexes containing viral RNA. We examined the potential influence of Toll-like receptors (TLRs), specifically TLR3 recognition of viral dsRNA exemplified by polyriboinosinic:polyribocytidylic acid [poly(I:C) RNA]. Normal human kidney stained positive for TLR3 on mesangial cells (MCs), vascular smooth muscle cells, and collecting duct epithelium. Cultured MCs have low TLR3 mRNA levels with predominant intracellular protein localization, which was increased by tumor necrosis factor-a, interleukin (IL)-1 beta, interferon (IFN)-gamma, and the TLR3 ligand poly(I:C) RNA. Poly(I:C) RNA stimulation of MCs increased mRNA and protein synthesis of IL-6, IL-1 beta, M-CSF, IL-8/CXCL8, RANTES/CCL5, MCP-1/CCL2, and ICAM-I; it also increased anti-proliferative and proapoptotic effects, the latter of which was decreased by inhibiting caspase-8. In microdissected glomeruli of normal and non-HCV membranoproliferative glomerulonephritis biopsies, TLR3 mRNA expression was low. in contrast TLR3 mRNA expression was significantly increased in hepatitis C-positive glomerulonephritis and was associated with enhanced mRNA for RANTES/CCL5 and MCP-1/CCL2. We hypothesize that immune complexes containing viral RNA activate mesangial TLR3 during HCV infection, thereby contributing to chemokine/cytokine release and effecting proliferation and apoptosis. Thus, TLR3 expression on renal cells, and especially MCs, may establish a link between viral infections and glomerular diseases
    Type of Publication: Journal article published
    PubMed ID: 16436653
    Signatur Availability
    BibTip Others were also interested in ...
  • 9
    ISSN: 1588-2837
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Description / Table of Contents: Abstract Кинетика окисления аскорбиновой кислоты ионами [(NH3)5RuORu(NH3)4ORu·(NH3)5]7+ была исследована методом остановленной струи. Были определены параметры активации и предлагается соответствующий механизм реакции.
    Notes: Abstract The kinetics of the oxidation of ascorbic acid by [(NH3)5RuORu(NH3)4ORu(NH3)5]7+ has been studied by the stopped-flow method. The activation parameters have been calculated and a possible mechanism is suggested.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 10
    ISSN: 1588-2837
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Description / Table of Contents: Abstract Исследовали кинетику восстановления комплекса (4,4,4-трифторо-1-(2-тионил)-бутандион-1,3)рутения(III) в метанольном растворе калиевой щелочи. На основе полученных результатов можно заключить, что во время реакции образуется промежуточный аддукт исследованного комплекса с метокси-ионом.
    Notes: Abstract Reduction of tris(4,4,4-trifluoro-1-(2-thienyl)-butane-1,3-dionato) ruthenium(III) in methanol solution containing potassium hydroxide has been studied kinetically. The results suggest outer-sphere complex formation between ruthenium(III) species and methoxide anion.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...