PMID- 10024304
OWN - NLM
STAT- MEDLINE
DCOM- 19990312
LR  - 20190706
IS  - 0009-7330 (Print)
IS  - 0009-7330 (Linking)
VI  - 84
IP  - 3
DP  - 1999 Feb 19
TI  - Anti-monocyte chemoattractant protein-1/monocyte chemotactic and activating 
      factor antibody inhibits neointimal hyperplasia in injured rat carotid arteries.
PG  - 306-14
AB  - Monocyte chemoattractant protein-1 (MCP-1)/monocyte chemotactic and activating 
      factor (MCAF) has been suggested to promote atherogenesis. The effects of in vivo 
      neutralization of MCP-1 in a rat model were examined in an effort to clarify the 
      role of MCP-1 in the development of neointimal hyperplasia. Competitive 
      polymerase chain reaction analysis revealed maximum MCP-1 mRNA expression at 4 
      hours after carotid arterial injury. Increased immunoreactivities of MCP-1 were 
      also detected at 2 and 8 hours after injury. Either anti-MCP-1 antibody or 
      nonimmunized goat IgG (10 mg/kg) was then administered every 12 hours to rats 
      that had undergone carotid arterial injury. Treatment with 3 consecutive doses of 
      anti-MCP-1 antibody within 24 hours (experiment 1) and every 12 hours for 5 days 
      (experiment 2) significantly inhibited neointimal hyperplasia at day 14, 
      resulting in a 27.8% reduction of the mean intima/media ratio (P<0.05) in 
      experiment 1 and a 43.6% reduction (P<0.01) in experiment 2. This effect was 
      still apparent at day 56 (55.6% inhibition; P<0.05). The number of vascular 
      smooth muscle cells in the neointima at day 4 was significantly reduced by 
      anti-MCP-1 treatment, demonstrating the important role of MCP-1 in early 
      neointimal lesion formation. However, recombinant MCP-1 did not stimulate 
      chemotaxis of vascular smooth muscle cells in an in vitro migration assay. These 
      results suggest that MCP-1 promotes neointimal hyperplasia in early neointimal 
      lesion formation and that neutralization of MCP-1 before, and immediately after, 
      arterial injury may be effective in preventing restenosis after angioplasty. 
      Further studies are needed to clarify the mechanism underlying the promotion of 
      neointimal hyperplasia by MCP-1.
FAU - Furukawa, Y
AU  - Furukawa Y
AD  - Department of Cardiovascular Medicine, Kyoto University Graduate School of 
      Medicine, Kyoto, Japan.
FAU - Matsumori, A
AU  - Matsumori A
FAU - Ohashi, N
AU  - Ohashi N
FAU - Shioi, T
AU  - Shioi T
FAU - Ono, K
AU  - Ono K
FAU - Harada, A
AU  - Harada A
FAU - Matsushima, K
AU  - Matsushima K
FAU - Sasayama, S
AU  - Sasayama S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Circ Res
JT  - Circulation research
JID - 0047103
RN  - 0 (Antibodies)
RN  - 0 (Chemokine CCL2)
SB  - IM
MH  - Animals
MH  - Antibodies/*immunology
MH  - Carotid Arteries/*pathology
MH  - Cell Movement
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics/immunology/*physiology
MH  - Hyperplasia
MH  - Macrophages/physiology
MH  - Male
MH  - Muscle, Smooth, Vascular/*pathology
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 1999/02/19 00:00
MHDA- 1999/02/19 00:01
CRDT- 1999/02/19 00:00
PHST- 1999/02/19 00:00 [pubmed]
PHST- 1999/02/19 00:01 [medline]
PHST- 1999/02/19 00:00 [entrez]
AID - 10.1161/01.res.84.3.306 [doi]
PST - ppublish
SO  - Circ Res. 1999 Feb 19;84(3):306-14. doi: 10.1161/01.res.84.3.306.