PMID- 10364084
OWN - NLM
STAT- MEDLINE
DCOM- 19990625
LR  - 20220409
IS  - 1079-5642 (Print)
IS  - 1079-5642 (Linking)
VI  - 19
IP  - 6
DP  - 1999 Jun
TI  - Monocyte chemoattractant protein-1 accelerates atherosclerosis in apolipoprotein 
      E-deficient mice.
PG  - 1518-25
AB  - The pro-inflammatory chemokine, monocyte chemoattractant protein-1 (MCP-1), plays 
      a fundamental role in monocyte recruitment and has been implicated as a 
      contributing factor to atherosclerosis. The predominant cell types within the 
      vessel wall--endothelial cells, smooth muscle cells, and macrophages--all 
      contribute to overexpression of MCP-1 in atherosclerotic tissue. In this report 
      we assess the role of MCP-1 expression by leukocytes on lesion progression in a 
      murine model susceptible to atherosclerosis. Bone marrow cells from mice 
      overexpressing a murine MCP-1 transgene on a background of apoE-deficiency or 
      from control mice were transplanted into irradiated apoE-knockout mice. After 
      repopulation of apoE-knockout mice with bone marrow containing the MCP-1 
      transgene, macrophages expressing the MCP-1 transgene were found in several 
      tissues, including the aorta. Qualitative assessment of atherosclerosis in these 
      mice revealed increased lipid staining, a 3-fold (P<0.001) increase in the amount 
      of oxidized lipid, and increased immunostaining for macrophage cell surface 
      markers with anti-F4/80 and anti-CD11b antibodies. There were no differences in 
      plasma lipids, plasma lipoprotein profiles, or body weight between the 2 groups. 
      These results provide the first direct evidence that MCP-1 expression by 
      leukocytes, predominately macrophages, increases the progression of 
      atherosclerosis by increasing both macrophage numbers and oxidized lipid 
      accumulation.
FAU - Aiello, R J
AU  - Aiello RJ
AD  - Department of Metabolic Disease, Central Research Division, Pfizer Inc, Groton, 
      Conn, USA. robert_j_aiello@groton.pfizer.com
FAU - Bourassa, P A
AU  - Bourassa PA
FAU - Lindsey, S
AU  - Lindsey S
FAU - Weng, W
AU  - Weng W
FAU - Natoli, E
AU  - Natoli E
FAU - Rollins, B J
AU  - Rollins BJ
FAU - Milos, P M
AU  - Milos PM
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Arterioscler Thromb Vasc Biol
JT  - Arteriosclerosis, thrombosis, and vascular biology
JID - 9505803
RN  - 0 (Apolipoproteins E)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lipids)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Macrophage-1 Antigen)
RN  - 0 (RNA, Messenger)
RN  - 0 (oxidized low density lipoprotein)
SB  - IM
MH  - Animals
MH  - Apolipoproteins E/*deficiency
MH  - Arteriosclerosis/*etiology
MH  - Chemokine CCL2/genetics/*physiology
MH  - Lipids/blood
MH  - Lipoproteins, LDL/metabolism
MH  - Macrophage-1 Antigen/analysis
MH  - Macrophages/chemistry
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - RNA, Messenger/analysis
EDAT- 1999/06/11 00:00
MHDA- 1999/06/11 00:01
CRDT- 1999/06/11 00:00
PHST- 1999/06/11 00:00 [pubmed]
PHST- 1999/06/11 00:01 [medline]
PHST- 1999/06/11 00:00 [entrez]
AID - 10.1161/01.atv.19.6.1518 [doi]
PST - ppublish
SO  - Arterioscler Thromb Vasc Biol. 1999 Jun;19(6):1518-25. doi: 
      10.1161/01.atv.19.6.1518.