PMID- 11382718
OWN - NLM
STAT- MEDLINE
DCOM- 20010719
LR  - 20190623
IS  - 1524-4539 (Electronic)
IS  - 0009-7322 (Linking)
VI  - 103
IP  - 21
DP  - 2001 May 29
TI  - Modulation of C-reactive protein-mediated monocyte chemoattractant protein-1 
      induction in human endothelial cells by anti-atherosclerosis drugs.
PG  - 2531-4
AB  - BACKGROUND: C-reactive protein (CRP) induces adhesion molecule expression by 
      endothelial cells. However, the effects of CRP on chemokine expression by 
      endothelial cells are not known. METHODS AND RESULTS: We tested the effects of 
      CRP on the production of the chemokines monocyte chemoattractant protein-1 
      (MCP-1) and RANTES in cultured human umbilical vein endothelial cells. The 
      secretion of chemokines was assessed by ELISA. Incubation with 100 microgram/mL 
      recombinant human CRP induced a 7-fold increase in MCP-1 but no change in RANTES 
      secretion. We showed that the effect of CRP on MCP-1 was present even at 5 
      microgram/mL CRP, with stepwise increases as the CRP concentration was increased 
      to 10, 50, and 100 microgram/mL. The effect of CRP on MCP-1 induction was not 
      influenced by aspirin (at concentrations up to 1 mmol/L), but it was 
      significantly inhibited by 5 micromol/L simvastatin. The peroxisome 
      proliferator-activated receptor-alpha activators fenofibrate (100 micromol/L) and 
      Wy-14649 (100 micromol/L) almost completely abolished the induction of MCP-1, but 
      the peroxisome proliferator-activated receptor-gamma activator ciglitazone had 
      only a moderate effect. CONCLUSIONS: These results further strengthen the role of 
      CRP in the pathogenesis of vascular inflammation and, likely, atherosclerosis and 
      provide a crucial insight into a novel mechanism of action of 
      anti-atherosclerosis drugs such as simvastatin and fenofibrate.
FAU - Pasceri, V
AU  - Pasceri V
AD  - Department of Cardiology, University of Texas-MD Anderson Cancer Center, Houston, 
      USA.
FAU - Cheng, J S
AU  - Cheng JS
FAU - Willerson, J T
AU  - Willerson JT
FAU - Yeh, E T
AU  - Yeh ET
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Circulation
JT  - Circulation
JID - 0147763
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Hypolipidemic Agents)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Transcription Factors)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - AGG2FN16EV (Simvastatin)
RN  - U202363UOS (Fenofibrate)
SB  - IM
EIN - Circulation 2001 Oct 16;104(16):1992. Chang J [corrected to Cheng JS]
MH  - C-Reactive Protein/*pharmacology
MH  - Cells, Cultured
MH  - Chemokine CCL2/*metabolism
MH  - Chemokine CCL5/metabolism
MH  - Dose-Response Relationship, Drug
MH  - Endothelium, Vascular/cytology/*drug effects/metabolism
MH  - Fenofibrate/pharmacology
MH  - Humans
MH  - Hypolipidemic Agents/*pharmacology
MH  - Receptors, Cytoplasmic and Nuclear/metabolism
MH  - Simvastatin/pharmacology
MH  - Time Factors
MH  - Transcription Factors/metabolism
EDAT- 2001/05/31 10:00
MHDA- 2001/07/20 10:01
CRDT- 2001/05/31 10:00
PHST- 2001/05/31 10:00 [pubmed]
PHST- 2001/07/20 10:01 [medline]
PHST- 2001/05/31 10:00 [entrez]
AID - 10.1161/01.cir.103.21.2531 [doi]
PST - ppublish
SO  - Circulation. 2001 May 29;103(21):2531-4. doi: 10.1161/01.cir.103.21.2531.