Linked Life Data

14514728

Source:http://linkedlifedata.com/resource/pubmed/id/14514728

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2003-9-29
pubmed:abstractText
Examined were CCR2-deficient mice to clarify the contribution of macrophages via monocyte chemoattractant protein 1 (MCP-1 or CCL2)/CCR2 signaling to the pathogenesis of renal ischemia-reperfusion injury. Also evaluated was the therapeutic effects via the inhibition of MCP-1/CCR2 signaling with propagermanium (3-oxygermylpropionic acid polymer) and RS-504393. Renal artery and vein of the left kidney were occluded with a vascular clamp for 60 min. A large number of infiltrated cells and marked acute tubular necrosis in outer medulla after renal ischemia-reperfusion injury was observed. Ischemia-reperfusion induced the expression of MCP-1 mRNA and protein in injured kidneys, followed by CCR2-positive macrophages in interstitium in wild-type mice. The expression of MCP-1 was decreased in CCR2-deficient mice compared with wild-type mice. The number of interstitial infiltrated macrophages was markedly smaller in the CCR2-deficient mice after ischemia-reperfusion. CCR2-deficient mice decreased the number of interstitial inducible nitric oxide synthase-positive cells after ischemia-reperfusion. The area of tubular necrosis in CCR2-deficient mice was significantly lower than that of wild-type mice after ischemia-reperfusion. In addition, CCR2-deficient mice diminished KC, macrophage inflammatory protein 2, epithelial cell-derived neutrophil-activating peptide 78, and neutrophil-activating peptide 2 expression compared with wild-type mice accompanied with the reduction of interstitial granulocyte infiltration. Similarly, propagermanium and RS-504393 reduced the number of interstitial infiltrated cells and tubular necrosis up to 96 h after ischemia-reperfusion injury. These results revealed that MCP-1 via CCR2 signaling plays a key role in the pathogenesis of renal ischemia-reperfusion injury through infiltration and activation of macrophages, and it offers a therapeutic target for ischemia-reperfusion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1046-6673
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2503-15
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:14514728-Animals, pubmed-meshheading:14514728-Chemokine CCL2, pubmed-meshheading:14514728-Chemotaxis, Leukocyte, pubmed-meshheading:14514728-Gene Expression, pubmed-meshheading:14514728-Granulocytes, pubmed-meshheading:14514728-Interferon Inducers, pubmed-meshheading:14514728-Kidney, pubmed-meshheading:14514728-Kidney Tubular Necrosis, Acute, pubmed-meshheading:14514728-Macrophages, pubmed-meshheading:14514728-Mice, pubmed-meshheading:14514728-Mice, Inbred C57BL, pubmed-meshheading:14514728-Mice, Inbred ICR, pubmed-meshheading:14514728-Nitric Oxide Synthase, pubmed-meshheading:14514728-Nitric Oxide Synthase Type II, pubmed-meshheading:14514728-Organometallic Compounds, pubmed-meshheading:14514728-RNA, Messenger, pubmed-meshheading:14514728-Receptors, CCR2, pubmed-meshheading:14514728-Receptors, Chemokine, pubmed-meshheading:14514728-Reperfusion Injury, pubmed-meshheading:14514728-Signal Transduction
pubmed:year
2003
pubmed:articleTitle
CCR2 signaling contributes to ischemia-reperfusion injury in kidney.
pubmed:affiliation
Department of Gastroenterology and Nephrology and Division of Blood Purification, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't