PMID- 10226098
OWN - NLM
STAT- MEDLINE
DCOM- 19990520
LR  - 20190623
IS  - 1524-4539 (Electronic)
IS  - 0009-7322 (Linking)
VI  - 99
IP  - 17
DP  - 1999 May 4
TI  - Monocyte chemoattractant protein-1 but not tumor necrosis factor-alpha is 
      correlated with monocyte infiltration in mouse lipid lesions.
PG  - 2310-6
AB  - BACKGROUND: Apolipoprotein (apo)(a) transgenic mice and C57BL/6 mice fed a high 
      fat diet develop similar-sized lipid lesions, but lesions in apo(a) mice are 
      devoid of macrophages. We used this observation to identify which proinflammatory 
      proteins might be involved in mediating monocyte recruitment during 
      atherogenesis. METHODS AND RESULTS: Macrophage-deficient apo(a) transgenic mouse 
      lesions contained similar levels of several different proinflammatory proteins, 
      both adhesion molecules (intercellular adhesion molecule-1 [ICAM-1] and vascular 
      cell adhesion molecule-1 [VCAM-1]) and cytokines (tumor necrosis factor-alpha 
      [TNF-alpha] and macrophage inflammatory protein-1alpha [MIP-1alpha]), similar to 
      the macrophage-rich lesions of C57BL/6 mice. CONCLUSIONS: From this we conclude 
      that ICAM-1, VCAM-1, TNF-alpha, and MIP-1alpha may all be necessary for vascular 
      monocyte recruitment in vivo, but they cannot be sufficient. Monocyte 
      chemoattractant protein-1 (MCP-1) protein was undetectable in the vessel wall 
      taken from apo(a) transgenic mice fed a high fat diet compared with high 
      expression in mice with lipid lesions (C57BL/6 and apoE knockout mice). Therefore 
      elevated expression of MCP-1 but not TNF-alpha, MIP-1alpha, ICAM-1, or VCAM-1 is 
      correlated with vascular macrophage accumulation. To test the hypothesis that 
      monocyte infiltration during atherogenesis is MCP-1 dependent, it will be 
      necessary to develop specific pharmacological inhibitors of MCP-1 activity.
FAU - Reckless, J
AU  - Reckless J
AD  - Departments of Biochemistry and Medicine, University of Cambridge, UK. 
      jr219@mole.bio.cam.ac.uk
FAU - Rubin, E M
AU  - Rubin EM
FAU - Verstuyft, J B
AU  - Verstuyft JB
FAU - Metcalfe, J C
AU  - Metcalfe JC
FAU - Grainger, D J
AU  - Grainger DJ
LA  - eng
GR  - Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Circulation
JT  - Circulation
JID - 0147763
RN  - 0 (Apolipoproteins)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Dietary Fats)
RN  - 0 (Lipoprotein(a))
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - EC 3.4.21.- (Apoprotein(a))
SB  - IM
MH  - Animals
MH  - Apolipoproteins/physiology
MH  - Apoprotein(a)
MH  - Arteriosclerosis/*pathology
MH  - Chemokine CCL2/*analysis
MH  - Dietary Fats/*toxicity
MH  - Female
MH  - Intercellular Adhesion Molecule-1/analysis
MH  - *Lipoprotein(a)
MH  - Macrophages/*pathology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Monocytes/*physiology
MH  - Tumor Necrosis Factor-alpha/*analysis
MH  - Vascular Cell Adhesion Molecule-1/analysis
EDAT- 1999/05/05 00:00
MHDA- 1999/05/05 00:01
CRDT- 1999/05/05 00:00
PHST- 1999/05/05 00:00 [pubmed]
PHST- 1999/05/05 00:01 [medline]
PHST- 1999/05/05 00:00 [entrez]
AID - 10.1161/01.cir.99.17.2310 [doi]
PST - ppublish
SO  - Circulation. 1999 May 4;99(17):2310-6. doi: 10.1161/01.cir.99.17.2310.