PMID- 14739122
OWN - NLM
STAT- MEDLINE
DCOM- 20050104
LR  - 20151119
IS  - 1524-4636 (Electronic)
IS  - 1079-5642 (Linking)
VI  - 24
IP  - 3
DP  - 2004 Mar
TI  - Monocyte chemoattractant protein-1 is an essential inflammatory mediator in 
      angiotensin II-induced progression of established atherosclerosis in 
      hypercholesterolemic mice.
PG  - 534-9
AB  - OBJECTIVE: Chronic inflammatory processes might be involved in the progression 
      and destabilization of atherosclerotic plaques. Therefore, identification of the 
      mechanism underlying arterial inflammatory function might lead to the development 
      of novel therapeutic strategies. Angiotensin II (AngII) is implicated in 
      atherogenesis by activating the vascular inflammation system, mainly through 
      monocyte chemotaxis. Therefore, we hypothesized that AngII increases plaque size 
      and promotes destabilization of established atheromas by activating the monocyte 
      chemoattractant protein-1 (MCP-1) pathway. METHODS AND RESULTS: We report here 
      that 4-week infusion of AngII not only increased plaque size but also induced a 
      destabilization phenotype (ie, increased macrophages and lipids and decreased 
      collagen and smooth muscle cells) of pre-existing atherosclerotic lesions of 
      hypercholesterolemic mice. AngII also enhanced the gene expression of 
      inflammatory cytokines (TNFalpha, IL-6, etc.) and chemokines (MCP-1, CCR2, etc). 
      Blockade of MCP-1, by transfecting the deletion mutant of the human MCP-1 gene 
      into the skeletal muscles, limited AngII-induced progression and destabilization 
      of established atherosclerotic lesions and suppressed the induction of 
      proinflammatory genes. CONCLUSIONS: These data suggest that MCP-1 functions as a 
      central inflammatory mediator in the AngII-induced progression and changes in 
      plaque composition of established atheroma.
FAU - Ni, Weihua
AU  - Ni W
AD  - Department of Cardiovascular Medicine, Graduate School of Medical Sciences, 
      Kyushu University, Fukuoka, Japan.
FAU - Kitamoto, Shiro
AU  - Kitamoto S
FAU - Ishibashi, Minako
AU  - Ishibashi M
FAU - Usui, Makoto
AU  - Usui M
FAU - Inoue, Shujiro
AU  - Inoue S
FAU - Hiasa, Ken-ichi
AU  - Hiasa K
FAU - Zhao, Qingwei
AU  - Zhao Q
FAU - Nishida, Ken-ichi
AU  - Nishida K
FAU - Takeshita, Akira
AU  - Takeshita A
FAU - Egashira, Kensuke
AU  - Egashira K
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20040122
PL  - United States
TA  - Arterioscler Thromb Vasc Biol
JT  - Arteriosclerosis, thrombosis, and vascular biology
JID - 9505803
RN  - 0 (Angiotensin II Type 1 Receptor Blockers)
RN  - 0 (Apolipoproteins E)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines)
RN  - 0 (Cytokines)
RN  - 0 (Imidazoles)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 0 (Tetrazoles)
RN  - 11128-99-7 (Angiotensin II)
RN  - 6M97XTV3HD (Olmesartan Medoxomil)
SB  - IM
MH  - Angiotensin II/administration & dosage/*toxicity
MH  - Angiotensin II Type 1 Receptor Blockers/pharmacology
MH  - Animals
MH  - Aortic Diseases/etiology/metabolism/pathology
MH  - Apolipoproteins E/deficiency/genetics
MH  - Arteriosclerosis/etiology/*metabolism/pathology
MH  - Chemokine CCL2/*physiology
MH  - Chemokines/biosynthesis/genetics
MH  - Cytokines/biosynthesis/genetics
MH  - Disease Progression
MH  - Gene Expression Regulation/drug effects
MH  - Gene Targeting
MH  - Humans
MH  - Hyperlipoproteinemia Type II/*complications
MH  - Imidazoles/pharmacology
MH  - Inflammation
MH  - Inflammation Mediators/*physiology
MH  - Injections, Intramuscular
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Olmesartan Medoxomil
MH  - Random Allocation
MH  - Recombinant Fusion Proteins/physiology
MH  - Sequence Deletion
MH  - Single-Blind Method
MH  - Tetrazoles/pharmacology
EDAT- 2004/01/24 05:00
MHDA- 2005/01/05 09:00
CRDT- 2004/01/24 05:00
PHST- 2004/01/24 05:00 [pubmed]
PHST- 2005/01/05 09:00 [medline]
PHST- 2004/01/24 05:00 [entrez]
AID - 01.ATV.0000118275.60121.2b [pii]
AID - 10.1161/01.ATV.0000118275.60121.2b [doi]
PST - ppublish
SO  - Arterioscler Thromb Vasc Biol. 2004 Mar;24(3):534-9. doi: 
      10.1161/01.ATV.0000118275.60121.2b. Epub 2004 Jan 22.