Chemokine receptor CCR1 but not CCR5 mediates leukocyte recruitment and subsequent renal fibrosis after unilateral ureteral obstruction
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11120%2F04%3A00000956" target="_blank" >RIV/00216208:11120/04:00000956 - isvavai.cz</a>
Result on the web
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DOI - Digital Object Identifier
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Alternative languages
Result language
angličtina
Original language name
Chemokine receptor CCR1 but not CCR5 mediates leukocyte recruitment and subsequent renal fibrosis after unilateral ureteral obstruction
Original language description
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
Czech name
Chemokinový receptor CCR1, na rozdíl od CCR5, zprostředkovává infiltraci intersticia lymfocyty a následnou fibrózu parenchymu ledviny po jednostranné obstrukci ureteru
Czech description
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.
Classification
Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
FP - Other medical fields
OECD FORD branch
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Result continuities
Project
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Continuities
S - Specificky vyzkum na vysokych skolach
Others
Publication year
2004
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Journal of American Society of Nephrology
ISSN
1046-6673
e-ISSN
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Volume of the periodical
15
Issue of the periodical within the volume
2
Country of publishing house
US - UNITED STATES
Number of pages
11
Pages from-to
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UT code for WoS article
000188604600011
EID of the result in the Scopus database
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