PMID- 16501303
OWN - NLM
STAT- MEDLINE
DCOM- 20060404
LR  - 20190819
IS  - 1346-9843 (Print)
IS  - 1346-9843 (Linking)
VI  - 70
IP  - 3
DP  - 2006 Mar
TI  - CC chemokine receptor-2 deficiency attenuates oxidative stress and infarct size 
      caused by myocardial ischemia-reperfusion in mice.
PG  - 342-51
AB  - BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1) and its major receptor, CC 
      chemokine receptor 2 (CCR2), have been shown to contribute to left ventricular 
      remodeling after myocardial infarction. However, it is unknown whether CCR2 
      deficiency protects the myocardium after myocardial ischemia-reperfusion. The 
      purpose of the present study was to investigate the effects of CCR2 deficiency on 
      myocardial ischemia-reperfusion injury in mice. METHODS AND RESULTS: Experiments 
      were performed in CCR2(-/-) and wild-type mice subjected to 45 min of ischemia 
      followed by reperfusion. Macrophage infiltration in ischemic lesions was markedly 
      reduced in CCR2(-/-) mice compared with wild-type mice (p<0.01). The infarct size 
      was significantly reduced in CCR2(-/-) mice compared with wild-type mice at 3 
      days after reperfusion (p<0.001). In situ zymography revealed augmented 
      gelatinolytic activity at 3 days after reperfusion in wild-type mice, but 
      significantly less activity in CCR2(-/-) mice. NADPH oxidase activity, the 
      intensity of nitrotyrosine staining and expression of inducible nitric oxide 
      synthase and thioredoxin-1 were significantly increased in ischemic myocardium in 
      wild-type mice compared with CCR2(-/-) mice, indicating a role for CCR2 in 
      oxidative stress after ischemia-reperfusion. CONCLUSIONS: Inhibition of the 
      MCP-1/CCR2 pathway may be a useful strategy for attenuating myocardial 
      ischemia-reperfusion injury.
FAU - Hayasaki, Takanori
AU  - Hayasaki T
AD  - Department of Cardiovascular Medicine, Graduate School of Medical Sciences, 
      Kumamoto University, Japan.
FAU - Kaikita, Koichi
AU  - Kaikita K
FAU - Okuma, Toshiyuki
AU  - Okuma T
FAU - Yamamoto, Eiichiro
AU  - Yamamoto E
FAU - Kuziel, William A
AU  - Kuziel WA
FAU - Ogawa, Hisao
AU  - Ogawa H
FAU - Takeya, Motohiro
AU  - Takeya M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Japan
TA  - Circ J
JT  - Circulation journal : official journal of the Japanese Circulation Society
JID - 101137683
RN  - 0 (Ccr2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Receptors, Chemokine)
RN  - EC 3.4.24.- (Matrix Metalloproteinases)
SB  - IM
MH  - Animals
MH  - Cell Movement/genetics/physiology
MH  - Chemokine CCL2/genetics/physiology
MH  - Cytokines/genetics/physiology
MH  - Gene Expression Regulation/physiology
MH  - Immunohistochemistry
MH  - Macrophages/chemistry/pathology/physiology
MH  - Male
MH  - Matrix Metalloproteinases/genetics/physiology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Monocytes/chemistry/pathology/physiology
MH  - Myocardial Infarction/*etiology/*pathology/physiopathology
MH  - Myocardial Reperfusion Injury/*complications/pathology/physiopathology
MH  - Myocardium/chemistry/pathology
MH  - Neutrophils/chemistry/pathology/physiology
MH  - Oxidative Stress/*physiology
MH  - RNA, Messenger/analysis/genetics
MH  - Receptors, CCR2
MH  - Receptors, Chemokine/analysis/*deficiency/genetics/physiology
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2006/02/28 09:00
MHDA- 2006/04/06 09:00
CRDT- 2006/02/28 09:00
PHST- 2006/02/28 09:00 [pubmed]
PHST- 2006/04/06 09:00 [medline]
PHST- 2006/02/28 09:00 [entrez]
AID - JST.JSTAGE/circj/70.342 [pii]
AID - 10.1253/circj.70.342 [doi]
PST - ppublish
SO  - Circ J. 2006 Mar;70(3):342-51. doi: 10.1253/circj.70.342.