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  • NEW-YORK  (4)
Keywords
  • 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
    Keywords: BLOOD ; Germany ; DENSITY ; HISTORY ; NEW-YORK ; PROTEIN ; PROTEINS ; HEART ; PATIENT ; kidney ; FAMILY ; antibodies ; antibody ; CLEAVAGE ; DELETION ; NO ; family history ; MUTATION ; PRESSURE ; BLOOD-PRESSURE ; ABNORMALITIES ; echocardiography ; FAILURE ; ultrasound ; SERUM ; DEFICIENCY ; FAMILIES ; LEVEL ; heparin ; FAMILY-HISTORY ; USA ; SYMPTOMS ; ARF ; FRAGMENT ; COMPLEMENT ; thrombotic thrombocytopenic purpura ; ACUTE-RENAL-FAILURE ; HUS
    Abstract: A 36-year-old patient complained of progressing fatigue, lack of appetite, and weakness for a few weeks, for which he had been using paracetamol (acetaminophen) intermittently. He was referred to our center from another hospital with hemolysis, thrombocytopenia, and acute renal failure (ARF). On admission, the patient did not complain of any specific additional symptoms. Besides paracetamol, he had not received any other medication. The patient reported flu-like symptoms 3 months before admission. The family history was unremarkable. Physical examination revealed a pale-looking patient (180 cm; 81 kg) with icteric sclerae. He was tachycardic (110 heart beats per min) and had elevated blood pressure (155/90mmHg). No other physical abnormalities were detectable. Laboratory investigations are depicted in Table 1. Specific analyses: von Willebrand factor cleavage protease activity 31% (40-120%), von Willebrand Factor Multimere negative, antibodies to von Willebrand Factor cleavage protease negative, factor H 614 mgl(-1) (345-590 mgl(-1)). Western blot analyses with patient's serum revealed the presence of complement factor H (CFH) and complement factor H-like protein 1 (CFHL1), but no detectable levels of complement factor H-related proteins 1 and 3 (CFHR1 and CFHR3) (Figure 1a). Antibodies to CFHR1 were negative. Genetic analyses 1 showed no CFH mutation, but revealed homozygous deletion of a 83 kb genomic fragment representing CFHR3 and CFHR1 (Figure 1b). Kidneys were of normal size with increased density by ultrasound examination. Electrocardiography revealed ischemic changes posteroseptally, and hypertrophy of the left ventricle was diagnosed by echocardiography
    Type of Publication: Journal article published
    PubMed ID: 18449173
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  • 4
    Keywords: CANCER ; human ; NEW-YORK ; ENZYMES ; MICE ; ACTIVATION ; kidney ; SUSCEPTIBILITY ; ACID ; HUMANS ; etiology ; METABOLIC-ACTIVATION ; FAILURE ; NEPHROPATHY ; INJURY ; aristolochic acid ; cytochrome P450 ; BALKAN ENDEMIC NEPHROPATHY ; DNA-ADDUCTS ; fibrosis ; urothelial cancer ; USA
    Abstract: Ingestion of aristolochic acid ( AA) is associated with the development of AA-nephropathy and Balkan endemic nephropathy, which are characterized by chronic renal failure, tubulointerstitial fibrosis, and urothelial cancer. Understanding which enzymes are involved in AA activation and/or detoxification is important in assessing susceptibility to AA. Xiao et al. demonstrate that hepatic cytochrome P450s in mice detoxicate AA and thereby protect kidney from injury. The relative contribution of enzymes activating AA to induce urothelial cancer in humans remains to be resolved
    Type of Publication: Journal article published
    PubMed ID: 18480852
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