PMID- 11282297
OWN - NLM
STAT- MEDLINE
DCOM- 20010521
LR  - 20191104
IS  - 1050-1738 (Print)
IS  - 1050-1738 (Linking)
VI  - 10
IP  - 5
DP  - 2000 Jul
TI  - Ligands for peroxisome proliferator-activated receptor inhibit monocyte CCR2 
      expression stimulated by plasma lipoproteins.
PG  - 209-16
AB  - Substantial evidence supports a causal role for monocyte chemoattractant 
      protein-1 (MCP-1) and its receptor, CCR2, in the recruitment of monocytes from 
      the circulation into atherosclerotic lesions. MCP-1 is produced and secreted by 
      virtually every cellular component of the vessel wall. It generally is assumed 
      that the magnitude of the monocyte chemotactic activity, which is initiated by 
      the functional activation of CCR2 by MCP-1, is directly proportional to the 
      concentration of the chemoattractant. However, we recently demonstrated that an 
      inflammatory response of monocytes is finely regulated and also depends on the 
      expression levels of CCR2. We identified plasma low-density lipoprotein (LDL) as 
      a positive regulator and showed that it greatly increased monocyte CCR2 gene 
      expression. In contrast, activation of peroxisome proliferator-activated receptor 
      by synthetic ligands or components of oxidized LDL reduces monocyte CCR2 
      expression and blocks chemotaxis mediated by MCP-1. We hypothesized that the 
      excessive monocyte accumulation in the vessel wall during atherogenesis may 
      result in part from an enhanced chemotactic response. These findings suggest CCR2 
      gene expression in circulating monocytes as a potential additional target for 
      intervention and prevention of atherosclerosis.
FAU - Han, K H
AU  - Han KH
AD  - Department of Medicine, University of California, San Diego, La Jolla, CA 92093, 
      USA.
FAU - Quehenberger, O
AU  - Quehenberger O
LA  - eng
GR  - HL56989/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - Trends Cardiovasc Med
JT  - Trends in cardiovascular medicine
JID - 9108337
RN  - 0 (CCR2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Ligands)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Receptors, Chemokine)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - Animals
MH  - Arteriosclerosis/*physiopathology
MH  - Chemokine CCL2
MH  - Humans
MH  - Ligands
MH  - Lipoproteins, LDL/*physiology
MH  - Receptors, CCR2
MH  - Receptors, Chemokine/*genetics
MH  - Receptors, Cytoplasmic and Nuclear/*physiology
MH  - Transcription Factors/*physiology
RF  - 40
EDAT- 2001/04/03 10:00
MHDA- 2001/05/30 10:01
CRDT- 2001/04/03 10:00
PHST- 2001/04/03 10:00 [pubmed]
PHST- 2001/05/30 10:01 [medline]
PHST- 2001/04/03 10:00 [entrez]
AID - S1050-1738(00)00076-1 [pii]
AID - 10.1016/s1050-1738(00)00076-1 [doi]
PST - ppublish
SO  - Trends Cardiovasc Med. 2000 Jul;10(5):209-16. doi: 10.1016/s1050-1738(00)00076-1.