PMID- 14644387
OWN - NLM
STAT- MEDLINE
DCOM- 20040826
LR  - 20190718
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 171
IP  - 2
DP  - 2003 Dec
TI  - Chylomicron remnants induce monocyte chemoattractant protein-1 expression via p38 
      MAPK activation in vascular smooth muscle cells.
PG  - 193-200
AB  - Chylomicron remnants, major lipoproteins at postprandial hyperlipidemia, have 
      been considered to be proatherogenic lipoproteins. However, the mechanisms by 
      which chylomicron remnants enhance atherosclerosis have not been fully 
      understood. Monocyte chemoattractant protein-1 (MCP-1) is a chemokine which 
      stimulates migration of monocytes and plays a critical role in the development of 
      atherosclerosis. In this study, we investigated the effect of chylomicron 
      remnants on MCP-1 expression in cultured vascular smooth muscle cells (VSMCs). We 
      prepared chylomicrons from the lymph of gastrostomized rats fed with egg solution 
      and obtained chylomicron remnants from the plasma of hepatectomized rats which 
      were injected with chylomicrons. Treatment of VSMC with chylomicron remnants 
      resulted in a significant increase of the expression of MCP-1 mRNA and protein in 
      a time-and a dose-dependent manner. Further, chylomicron remnants activated p38 
      mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase 
      (ERK1/2). Pretreatment of VSMCs with p38 MAPK inhibitors, SB203580 and SB202190, 
      resulted in a dose-dependent inhibition of chylomicron remnants-induced MCP-1 
      mRNA and protein expression, whereas a MAPK kinase inhibitor, PD98059, had no 
      effect on these responses. MCP-1 secretion by chylomicron remnants was much more 
      pronounced than those by chylomicrons, oxidized low-density lipoproteins, or 
      lysophosphatidylcholine. These results indicated that chylomicron remnants 
      stimulated MCP-1 expression in VSMCs, and suggested that chylomicron remnants 
      might contribute to the formation of atherosclerosis through this proinflammatory 
      effect.
CI  - Copyright 2003 Elsevier Ireland Ltd.
FAU - Domoto, Koji
AU  - Domoto K
AD  - Division of Cardiovascular and Respiratory Medicine, Department of Internal 
      Medicine, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki-cho, 
      Chuo-ku, 650-0017, Kobe, Japan.
FAU - Taniguchi, Takahiro
AU  - Taniguchi T
FAU - Takaishi, Hiroshi
AU  - Takaishi H
FAU - Takahashi, Tomosaburo
AU  - Takahashi T
FAU - Fujioka, Yoshio
AU  - Fujioka Y
FAU - Takahashi, Akihiro
AU  - Takahashi A
FAU - Ishikawa, Yuichi
AU  - Ishikawa Y
FAU - Yokoyama, Mitsuhiro
AU  - Yokoyama M
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chylomicron Remnants)
RN  - 0 (Chylomicrons)
RN  - 63231-63-0 (RNA)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
SB  - IM
MH  - Animals
MH  - Arteriosclerosis/pathology/physiopathology
MH  - Blotting, Northern
MH  - Cell Survival
MH  - Cells, Cultured
MH  - Chemokine CCL2/analysis/*metabolism
MH  - Chylomicron Remnants
MH  - Chylomicrons/*pharmacology
MH  - Disease Models, Animal
MH  - MAP Kinase Signaling System
MH  - Male
MH  - Mitogen-Activated Protein Kinase 1/*drug effects/*metabolism
MH  - Muscle, Smooth, Vascular/*cytology
MH  - RNA/analysis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sensitivity and Specificity
EDAT- 2003/12/04 05:00
MHDA- 2004/08/27 05:00
CRDT- 2003/12/04 05:00
PHST- 2003/12/04 05:00 [pubmed]
PHST- 2004/08/27 05:00 [medline]
PHST- 2003/12/04 05:00 [entrez]
AID - S0021-9150(03)00355-1 [pii]
AID - 10.1016/j.atherosclerosis.2003.08.016 [doi]
PST - ppublish
SO  - Atherosclerosis. 2003 Dec;171(2):193-200. doi: 
      10.1016/j.atherosclerosis.2003.08.016.