Source:http://linkedlifedata.com/resource/pubmed/id/15034096
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2004-3-22
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pubmed:abstractText |
Monocyte chemoattractant protein (MCP)-1, also termed monocyte chemotactic and activating factor (MCAF)/CCL2, plays an important role in progressive organ fibrosis. It was hypothesized that MCP-1, through its cognate receptor, CCR2, regulates the pathogenesis and is therapeutically of importance for renal fibrosis. To achieve this goal, the therapeutic efficacy and efficiency in renal fibrosis induced by a unilateral ureteral obstruction nephropathy model in mice by the blockade of MCP-1/CCR2 signaling was studied. The delivery of N-terminal deletion mutant of the human MCP-1 gene, 7ND, into a skeletal muscle ameliorated renal fibrosis by resulting in decrease in the deposit of type I collagen and in reduced expression of TGF-beta. Concomitantly, gene transfer of 7ND reduced the cell infiltration, most of which were CCR2-positive macrophages, followed by the decrease in MCP-1 expression in the diseased kidneys. These observations suggest that MCP-1 through CCR2 signaling is responsible for Mphi recruitment, which augments downstream events, resulting in renal fibrosis. Moreover, these findings imply that gene therapy against MCP-1/CCR2 signaling via the mutant gene transferred strategy may serve a beneficial therapeutic application for renal fibrosis.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CCR2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Ccr2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1046-6673
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pubmed:author |
pubmed-author:EgashiraKensukeK,
pubmed-author:FuruichiKengoK,
pubmed-author:HashimotoHiroyukiH,
pubmed-author:IshidaYukoY,
pubmed-author:IshiwataYoshiroY,
pubmed-author:IwataYasunoriY,
pubmed-author:KitagawaKiyokiK,
pubmed-author:KondoToshikazuT,
pubmed-author:MatsushimaKoujiK,
pubmed-author:MukaidaNaofumiN,
pubmed-author:SakaiNorihikoN,
pubmed-author:TomosugiNaohisaN,
pubmed-author:WadaTakashiT,
pubmed-author:YokoyamaHitoshiH
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pubmed:issnType |
Print
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pubmed:volume |
15
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
940-8
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:15034096-Animals,
pubmed-meshheading:15034096-Chemokine CCL2,
pubmed-meshheading:15034096-Fibrosis,
pubmed-meshheading:15034096-Gene Therapy,
pubmed-meshheading:15034096-Kidney,
pubmed-meshheading:15034096-Kidney Diseases,
pubmed-meshheading:15034096-Male,
pubmed-meshheading:15034096-Mice,
pubmed-meshheading:15034096-Mice, Inbred BALB C,
pubmed-meshheading:15034096-Mutation,
pubmed-meshheading:15034096-Receptors, CCR2,
pubmed-meshheading:15034096-Receptors, Chemokine
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pubmed:year |
2004
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pubmed:articleTitle |
Gene therapy via blockade of monocyte chemoattractant protein-1 for renal fibrosis.
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pubmed:affiliation |
Department of Gastroenterology and Nephrology, Graduate School of Medical Science and Division of Blood Purification, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan. twada@medf.m.kanazawa-u.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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