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  • CELLS  (6)
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  • 1
    Keywords: RECEPTOR ; CELLS ; CELL ; Germany ; human ; MICROSCOPY ; NEW-YORK ; HYBRIDIZATION ; PROTEIN ; PROTEINS ; ACTIVATION ; kidney ; IN-SITU ; immunohistochemistry ; UP-REGULATION ; COMPONENT ; PCR ; EPITHELIAL-CELLS ; POLYMERASE-CHAIN-REACTION ; immune response ; IMMUNE-RESPONSE ; CHAIN-REACTION ; REJECTION ; SEGMENTS ; LOCATION ; TNF-ALPHA ; in situ hybridization ; CYTOKINE ; CHAIN ; secretion ; polymerase chain reaction ; BLOOD MONONUCLEAR-CELLS ; INTERCELLULAR-ADHESION MOLECULE-1 ; USA ; immunology ; distal tubule ; ACUTE TUBULAR-NECROSIS ; collecting ducts ; CONNECTING TUBULE ; CYTOKINE RESPONSES ; GAMMA-INDUCING FACTOR ; INTERLEUKIN-18
    Abstract: We determined the cellular location of interleukin-18 (IL-18) and caspase-1 and the purinergic receptor P2X7, two proteins necessary for its activation and secretion. The mRNA and protein of IL-18 were detectable in normal human kidney by means of polymerase chain reaction (PCR), in situ hybridization, and Western blot. Immunohistochemistry located IL-18 to nephron segments containing calbinbin-D28k or aquaporin-2 that suggest location in the distal convoluted and the connecting tubule and to parts of the collecting duct. IL-18 was not detected in the thick ascending limb of Henle. Confocal microscopy showed that IL-18 was expressed in cells negative for calbindin-D28k and for aquaporin-2 but positive for the vacuolar H+ -ATPase. This demonstrates that the intercalated cells produce IL-18. These segments were also positive for caspase-1 and P2X7 that are essential for IL-18 secretion. Our results show that IL-18 is constitutively expressed by intercalated cells of the late distal convoluted tubule, the connecting tubule, and the collecting duct of the healthy human kidney. Since IL-18 is an early component of the inflammatory cytokine cascade, its location suggests that renal intercalated cells may contribute to immediate immune response of the kidney
    Type of Publication: Journal article published
    PubMed ID: 17687255
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  • 2
    Keywords: CANCER ; CELLS ; EXPRESSION ; tumor ; BLOOD ; CELL ; Germany ; NEW-YORK ; PROTEIN ; MICE ; RELEASE ; kidney ; MARKER ; ANTIGEN ; T-CELLS ; treatment ; CLEAVAGE ; knockout ; MEMBRANE ; WOMEN ; SURFACE ; INDIVIDUALS ; L1 ; CALCIUM ; BODY ; ADHESION MOLECULE ; membrane vesicles ; MEMBRANE-VESICLES ; CD24 ; URINE ; AGENT ; BODIES ; RE ; VESICLES ; secretion ; interaction ; KNOCKOUT MICE ; USA ; BIOGENESIS ; PODOCYTES ; exosome ; OVARIAN-CARCINOMA CELLS ; exosomes ; amniotic fluid ; INFANT
    Abstract: Exosomes are small membrane vesicles that are secreted from a variety of cell types into various body fluids including the blood and urine. These vesicles are thought to play a role in cell-cell interactions. CD24 is a small but extensively glycosylated protein linked to the cell surface by means of a glycosyl-phosphatidylinositol anchor. In this study we found that CD24 is present in membrane vesicles characterized as exosomes that were isolated from the urine of normal individuals. CD24 was expressed by both tubule cells and podocytes and treatment of the latter with a cholesterol-extracting agent, but not with a calcium ionophore, caused the release of CD24-containing exosomes. Using CD24 as a marker, we found exosomes in the urine of newborn infants and in the amniotic fluid of pregnant women with similar findings made in mice. Interestingly, studies with CD24 knockout mice showed that the exosomes are released from the fetus but not from the mother; however, exosome release was similar from both the knockout and the wild-type mice. This indicates that CD24 is not essential for exosome formation or release but may be a convenient exosome marker. Our studies suggest that exosomal secretion from the embryonic kidney could play a biological role at the fetal-maternal interphase
    Type of Publication: Journal article published
    PubMed ID: 17700640
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  • 3
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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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  • 4
    Keywords: CELLS ; EXPRESSION ; tumor ; TUMOR-CELLS ; carcinoma ; CELL ; human ; GENE ; PROTEIN ; TUMORS ; MECHANISM ; renal ; CARCINOGENESIS ; mechanisms ; DOWN-REGULATION ; SIGNAL ; STAGE ; immunohistochemistry ; MEMBRANE ; MUTATION ; TUMOR-SUPPRESSOR GENE ; MUTATIONS ; LOCALIZATION ; CARCINOMAS ; DECLINE ; VON-HIPPEL-LINDAU ; protein expression ; HUMAN TISSUES ; RENAL-CELL CARCINOMA ; von Hippel-Lindau,immunohistochemistry,down-regulation,localization,membrane,renal tumor
    Abstract: Background. The von Hippel-Lindau (VHL) gene has been widely analyzed in many tumors. Early studies in animal tumors suggest that changes in VHL protein level and localization may be also important in tumorigenesis. In this study, we determined the role of VHL protein in human renal cell carcinomas.Methods. Seventy-five human renal cell carcinomas, predominantly of clear cell type (60 of 75), were examined for VHL protein by immunohistochemistry. The level and pattern of protein expression were then compared to VHL mutations and tumor characteristics.Results. An apparent decline of VHL level (positive in 〈50% of tumor cells) was observed in 49 (65%) tumors, a change more frequent than VHL mutations (28 of 75) (37%). In tumors, VHL was localized to the cytoplasm and/or the cell membrane. The occurrence of a predominantly membranous signal was significantly associated with missense mutations (9 of 14 tumors with missense mutations versus 14 of 61 tumors with no or nonmissense mutations, P = 0.0025) and tumor stage (23 of 60 tumors with stage TI versus 0 of 15 tumors with TII and TIII, P = 0.0034).Conclusion. This study provides the first evidence of the role of VHL protein level and intracellular localization in tumorigenesis in humans
    Type of Publication: Journal article published
    PubMed ID: 14531799
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  • 5
    Keywords: ANGIOGENESIS ; CELLS ; EXPRESSION ; GROWTH ; GROWTH-FACTOR ; CELL ; Germany ; human ; PATHWAYS ; SYSTEM ; GENE ; GENES ; PROTEIN ; transcription ; kidney ; TRANSCRIPTION FACTOR ; RAT ; CONTRAST ; ALPHA ; TARGET ; STAGE ; TRANSCRIPTION FACTORS ; TRANSGENIC MICE ; LOCALIZATION ; OXYGEN ; ALPHA-SUBUNIT ; ERYTHROPOIETIN ; VEGF ; LACKING ; HYPOXIA ; development ; LEVEL ; NUCLEAR ; MATURE ; branching ; DUCT ; EPAS1 ; glomerulogenesis ; GLYCOLYSIS ; HIF ; HIF-1 ; HIF-ALPHA ; HOMEOSTASIS ; kidney development ; nephrogenesis ; podocyte ; PODOCYTES ; TUBULOGENESIS ; vasculogenesis
    Abstract: Early kidney development is associated with the coordinated branching of the renal tubular and vascular system and hypoxia has been proposed to be a major regulatory factor in this process. Under low oxygen levels, the hypoxia-inducible transcription factor (HIF) regulates the expression of genes involved in angiogenesis, erythropoiesis and glycolysis. To investigate the role of HIF in kidney development, we analyzed the temporal and spatial expression of the oxygen regulated HIF-1 alpha and -2 alpha subunits at different stages of rat and human kidney development. Using double-staining procedures, localization of the HIF target geneproducts vascular endothelial growth factor (VEGF) and endoglin was studied in relation to HIF alpha. In both species, we found marked nuclear expression of HIF-1 alpha in medullary and cortical collecting ducts and in glomerular cells. In contrast, HIF-2 alpha was expressed in interstitial and peritubular cells podocytes of the more mature glomeruli. After completion of glomerulogenesis and nephrogenesis, HIF-1 alpha and -2 alpha were no longer detectable. The HIF-target gene VEGF colocalized with HIF-1 alpha protein in glomeruli and medullary collecting ducts. HIF-2 alpha colocalized with the endothelium-associated angiogenic factor, endoglin. Both HIF alpha isoforms are activated in the developing kidney in a cell-specific and temporally controlled manner, indicating a regulatory role of oxygen tension in nephrogenesis. HIF-1 alpha seems to be primarily involved in tubulogenesis and HIF-2 alpha in renal vasculogenesis. Both isoforms are found in glomerulogenesis, potentially having synergistic effects
    Type of Publication: Journal article published
    PubMed ID: 16374431
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  • 6
    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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