PMID- 22664781
OWN - NLM
STAT- MEDLINE
DCOM- 20130201
LR  - 20220309
IS  - 1347-4820 (Electronic)
IS  - 1346-9843 (Linking)
VI  - 76
IP  - 9
DP  - 2012
TI  - Independent roles of monocyte chemoattractant protein-1, regulated on activation, 
      normal T-cell expressed and secreted and fractalkine in the vulnerability of 
      coronary atherosclerotic plaques.
PG  - 2167-73
AB  - BACKGROUND: Monocyte chemotactic factors contribute to the formation of 
      atherosclerotic plaques. The present study aimed to elucidate the roles of 
      monocyte chemoattractant protein-1 (MCP-1), Regulated on Activation, Normal 
      T-cell Expressed and Secreted (RANTES) and fractalkine on the vulnerability of 
      atherosclerotic plaques in patients with acute myocardial infarction (AMI) or 
      unstable angina pectoris (UAP). METHODS AND RESULTS: Sixty patients with AMI, 60 
      patients with UAP, 60 patients with stable angina pectoris (SAP) and 40 patients 
      without coronary heart disease comprised the study group. Quantitative coronary 
      angiography and intravascular ultrasound (IVUS) were performed. Concentrations 
      and mRNA expression levels of high-sensitivity C-reactive protein, MCP-1, RANTES 
      and fractalkine were measured by ELISA and RT-PCR, respectively. IVUS found that 
      51.3% of the AMI patients and 47.7% of the UAP patients had soft lipid plaques. 
      Among the SAP patients, 52.4% had fibrous plaques and only 17.1% had soft 
      plaques. AMI and UAP patients had larger plaque burden and vascular remodeling 
      index than did the SAP patients (P<0.01). The averaged number of migrated 
      monocytes was higher in AMI and UAP patients. Concentrations and mRNA expression 
      levels of MCP-1, RANTES and fractalkine were significantly higher in AMI and UAP 
      patients than in SAP patients (P<0.05-0.01). The plaque burden in UAP patients as 
      measured with IVUS correlated well with monocytes chemotaxis (r=0.56, P<0.01). 
      CONCLUSIONS: MCP-1, RANTES and fractalkine independently participate in the 
      pathogenesis of plaque vulnerability and subsequent plaque rupture.  
FAU - Li, Jifu
AU  - Li J
AD  - The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese 
      Ministry of Education and Chinese Ministry of Health, Shandong University Qilu 
      Hospital, Shandong, PR China.
FAU - Guo, Yuan
AU  - Guo Y
FAU - Luan, Xiaorong
AU  - Luan X
FAU - Qi, Tianjun
AU  - Qi T
FAU - Li, Daqing
AU  - Li D
FAU - Chen, Yuguo
AU  - Chen Y
FAU - Ji, Xiaoping
AU  - Ji X
FAU - Zhang, Yun
AU  - Zhang Y
FAU - Chen, Wenqiang
AU  - Chen W
LA  - eng
PT  - Clinical Trial
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120605
PL  - Japan
TA  - Circ J
JT  - Circulation journal : official journal of the Japanese Circulation Society
JID - 101137683
RN  - 0 (CCL2 protein, human)
RN  - 0 (CCL5 protein, human)
RN  - 0 (CX3CL1 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Chemokine CX3CL1)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Angina, Unstable/blood/complications/diagnostic imaging
MH  - C-Reactive Protein/metabolism
MH  - Chemokine CCL2/*blood
MH  - Chemokine CCL5/*blood
MH  - Chemokine CX3CL1/*blood
MH  - Coronary Angiography
MH  - Coronary Artery Disease/*blood/complications/diagnostic imaging
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/blood/complications/diagnostic imaging
MH  - Plaque, Atherosclerotic/*blood/complications/diagnostic imaging
MH  - Ultrasonography, Interventional
EDAT- 2012/06/06 06:00
MHDA- 2013/02/05 06:00
CRDT- 2012/06/06 06:00
PHST- 2012/06/06 06:00 [entrez]
PHST- 2012/06/06 06:00 [pubmed]
PHST- 2013/02/05 06:00 [medline]
AID - DN/JST.JSTAGE/circj/CJ-11-1457 [pii]
AID - 10.1253/circj.cj-11-1457 [doi]
PST - ppublish
SO  - Circ J. 2012;76(9):2167-73. doi: 10.1253/circj.cj-11-1457. Epub 2012 Jun 5.