PMID- 9118522
OWN - NLM
STAT- MEDLINE
DCOM- 19970424
LR  - 20220410
IS  - 0009-7322 (Print)
IS  - 0009-7322 (Linking)
VI  - 95
IP  - 6
DP  - 1997 Mar 18
TI  - Angiotensin-converting enzyme inhibition prevents arterial nuclear factor-kappa B 
      activation, monocyte chemoattractant protein-1 expression, and macrophage 
      infiltration in a rabbit model of early accelerated atherosclerosis.
PG  - 1532-41
AB  - BACKGROUND: The migration of monocytes into the vessel wall is a critical event 
      leading to the development of atherosclerosis. Monocyte chemoattractant protein-1 
      (MCP-1) is the main chemotactic factor involved in this phenomenon, and nuclear 
      factor-kappa B (NF-kappa B) is one of the nuclear factors controlling its 
      expression. ACE inhibitors have been useful in some experimental models of 
      atherosclerosis. In this work, we addressed the hypothesis that angiotensin II 
      (Ang II) may be implicated in the recruitment of monocytes into the vessel wall 
      through the activation of NF-kappa B and the induction of MCP-1 expression. 
      METHODS AND RESULTS: Accelerated atherosclerosis was induced in the femoral 
      arteries of rabbits by endothelial desiccation and atherogenic diet for 7 days. 
      Atherosclerotic vessels exhibited an increase in NF-kappa B-like activity, and 
      p50 and p65 NF-kappa B subunits were identified as components of this activity. 
      MCP-1 (mRNA and protein) was also expressed in the injured vessels coincidently 
      with the neointimal macrophage infiltration. ACE inhibition with quinapril 
      reduced these three parameters. In cultured monocytic and vascular smooth muscle 
      cells. Ang II elicited an increase in NF-kappa B activation and MCP-1 expression 
      that was prevented by preincubation of cells with pyrrolidinedithiocarbamate, an 
      inhibitor of NF-kappa B activation. CONCLUSIONS: The present data support a role 
      for Ang II in neointimal monocyte infiltration through NF-kappa B activation and 
      MCP-1 expression in a model of accelerated atherosclerosis in rabbits. Our 
      results suggest that ACE inhibitors may have a beneficial effect in early 
      atherosclerosis.
FAU - Hernandez-Presa, M
AU  - Hernandez-Presa M
AD  - Research Laboratory, Fundacion Jimenez Diaz, Autonoma University, Madrid, Spain.
FAU - Bustos, C
AU  - Bustos C
FAU - Ortego, M
AU  - Ortego M
FAU - Tunon, J
AU  - Tunon J
FAU - Renedo, G
AU  - Renedo G
FAU - Ruiz-Ortega, M
AU  - Ruiz-Ortega M
FAU - Egido, J
AU  - Egido J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Circulation
JT  - Circulation
JID - 0147763
RN  - 0 (Angiotensin-Converting Enzyme Inhibitors)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Isoquinolines)
RN  - 0 (NF-kappa B)
RN  - 0 (Tetrahydroisoquinolines)
RN  - EC 3.4.15.1 (Peptidyl-Dipeptidase A)
RN  - RJ84Y44811 (Quinapril)
SB  - IM
MH  - Angiotensin-Converting Enzyme Inhibitors/*pharmacology
MH  - Animals
MH  - Arteriosclerosis/*metabolism/pathology/*physiopathology
MH  - Cell Movement/drug effects
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Femoral Artery/*metabolism/pathology
MH  - Gene Expression
MH  - Immunohistochemistry
MH  - Isoquinolines/pharmacology
MH  - Macrophages/*drug effects/physiology
MH  - Male
MH  - Monocytes/metabolism/physiology
MH  - Muscle, Smooth, Vascular/metabolism/pathology/physiology
MH  - NF-kappa B/*drug effects/physiology
MH  - Peptidyl-Dipeptidase A/metabolism
MH  - Quinapril
MH  - Rabbits
MH  - *Tetrahydroisoquinolines
EDAT- 1997/03/18 00:00
MHDA- 1997/03/18 00:01
CRDT- 1997/03/18 00:00
PHST- 1997/03/18 00:00 [pubmed]
PHST- 1997/03/18 00:01 [medline]
PHST- 1997/03/18 00:00 [entrez]
AID - 10.1161/01.cir.95.6.1532 [doi]
PST - ppublish
SO  - Circulation. 1997 Mar 18;95(6):1532-41. doi: 10.1161/01.cir.95.6.1532.