About: Chemokine receptor CCR1 but not CCR5 mediates leukocyte recruitment and subsequent renal fibrosis after unilateral ureteral obstruction     Goto   Sponge   NotDistinct   Permalink

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  • As chemokine receptor CCR1 and CCR5 expression on circulating leukocytes is thought to contribute to leukocyte recruitment during renal fibrosis, the authors examined the effects of unilateral ureteral obstruction (UUO) in mice deficient for CCR1 or CCR5. Analysis of UUO kidneys from CCR1-deficient mice revealed a reduction of interstitial macrophages and lymphocytes (35% and 55%, respectively) compared with wild-type controls. CCR1-deficient mice had reduced CCR5 mRNA levels in UUO kidneys, which correlated with a reduction of CCR5+ T cell infiltrate as determined by flow cytometry. Interstitial fibroblasts, renal TGF-beta1 mRNA expression, interstitial volume, and collagen I deposits were all significantly reduced in CCR1-deficient mice. In contrast, renal leukocytes and fibrosis were unaffected in CCR5-deficient mice with UUO. However, if treated with the CCR1 antagonist BX471, CCR5-deficient mice showed a similar reduction of renal leukocytes and fibrosis as CCR1-deficient mice. To determine the u
  • As chemokine receptor CCR1 and CCR5 expression on circulating leukocytes is thought to contribute to leukocyte recruitment during renal fibrosis, the authors examined the effects of unilateral ureteral obstruction (UUO) in mice deficient for CCR1 or CCR5. Analysis of UUO kidneys from CCR1-deficient mice revealed a reduction of interstitial macrophages and lymphocytes (35% and 55%, respectively) compared with wild-type controls. CCR1-deficient mice had reduced CCR5 mRNA levels in UUO kidneys, which correlated with a reduction of CCR5+ T cell infiltrate as determined by flow cytometry. Interstitial fibroblasts, renal TGF-beta1 mRNA expression, interstitial volume, and collagen I deposits were all significantly reduced in CCR1-deficient mice. In contrast, renal leukocytes and fibrosis were unaffected in CCR5-deficient mice with UUO. However, if treated with the CCR1 antagonist BX471, CCR5-deficient mice showed a similar reduction of renal leukocytes and fibrosis as CCR1-deficient mice. To determine the u (en)
  • Chemokinové receptory CCR1 a CCR5 na cirkulujících leukocytech přispívají k infiltraci ledvinného parenchymu leukocyty a k následné fibróze intrasticia ledviny. Autoři zkoumali efekt jednostanné obstrukce močovodu u myší s defektem CCR1 a CCR5. U CCR1 defektních myší došlo k redukci počtu infiltrujících lymfocytů a makrofágů v intersticiu, počtu fibroblastů, objemu intersticia a hladině mRNA TGF-beta1, v provnání s divokým kmenem. Obdobné výsledky byly zaznamenány u myší CCR5 deficientních léčených BX 471, antagonistou CCR1. CCR5 deficientní myši vyvinuly po obstrukci ureteru fibrózu stejného rozsahu jako divoký kmen myší. CCR1 je potenciálně vhodným cílem léčebné strategie fibrózy intersticia ledviny. (cs)
Title
  • Chemokine receptor CCR1 but not CCR5 mediates leukocyte recruitment and subsequent renal fibrosis after unilateral ureteral obstruction
  • Chemokine receptor CCR1 but not CCR5 mediates leukocyte recruitment and subsequent renal fibrosis after unilateral ureteral obstruction (en)
  • Chemokinový receptor CCR1, na rozdíl od CCR5, zprostředkovává infiltraci intersticia lymfocyty a následnou fibrózu parenchymu ledviny po jednostranné obstrukci ureteru (cs)
skos:prefLabel
  • Chemokine receptor CCR1 but not CCR5 mediates leukocyte recruitment and subsequent renal fibrosis after unilateral ureteral obstruction
  • Chemokine receptor CCR1 but not CCR5 mediates leukocyte recruitment and subsequent renal fibrosis after unilateral ureteral obstruction (en)
  • Chemokinový receptor CCR1, na rozdíl od CCR5, zprostředkovává infiltraci intersticia lymfocyty a následnou fibrózu parenchymu ledviny po jednostranné obstrukci ureteru (cs)
skos:notation
  • RIV/00216208:11120/04:00000956!RIV09-MSM-11120___
http://linked.open...avai/riv/aktivita
http://linked.open...avai/riv/aktivity
  • S
http://linked.open...iv/cisloPeriodika
  • 2
http://linked.open...vai/riv/dodaniDat
http://linked.open...aciTvurceVysledku
http://linked.open.../riv/druhVysledku
http://linked.open...iv/duvernostUdaju
http://linked.open...titaPredkladatele
http://linked.open...dnocenehoVysledku
  • 557576
http://linked.open...ai/riv/idVysledku
  • RIV/00216208:11120/04:00000956
http://linked.open...riv/jazykVysledku
http://linked.open.../riv/klicovaSlova
  • macrophage-inflammatory protein-1-alpha; interstitial fibrosis; transplant rejection; host-defense; mice lacking; expression; antagonist; glomerulonephritis; infiltration; nephropathy (en)
http://linked.open.../riv/klicoveSlovo
http://linked.open...odStatuVydavatele
  • US - Spojené státy americké
http://linked.open...ontrolniKodProRIV
  • [AC8F8D02ADD5]
http://linked.open...i/riv/nazevZdroje
  • Journal of American Society of Nephrology
http://linked.open...in/vavai/riv/obor
http://linked.open...ichTvurcuVysledku
http://linked.open...cetTvurcuVysledku
http://linked.open...UplatneniVysledku
http://linked.open...v/svazekPeriodika
  • 15
http://linked.open...iv/tvurceVysledku
  • Eis, Václav
  • Mack, M.
  • Schlöndorff, D.
  • Anders, H. J.
  • Luckow, B.
  • Vielhauer, V.
  • Kretzler, M.
  • Linde, Y.
  • Perez de Lema, G.
  • Alpers, C. E.
  • Cohen, C. D.
  • Gao, J. L.
  • Gröne, H. J.
  • Horuk, R.
  • Hudkins, K. L.
  • Murphy, P. M.
  • Segerer, S.
  • Sireke, J.
http://linked.open...ain/vavai/riv/wos
  • 000188604600011
issn
  • 1046-6673
number of pages
http://localhost/t...ganizacniJednotka
  • 11120
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