PMID- 16834927
OWN - NLM
STAT- MEDLINE
DCOM- 20060809
LR  - 20161124
IS  - 0366-6999 (Print)
IS  - 0366-6999 (Linking)
VI  - 119
IP  - 13
DP  - 2006 Jul 5
TI  - Advanced oxidation protein products induce monocyte chemoattractant protein-1 
      expression via p38 mitogen-activated protein kinase activation in rat vascular 
      smooth muscle cells.
PG  - 1088-93
AB  - BACKGROUND: Advanced oxidation protein products (AOPPs) are new uremic toxins 
      reported by Witko-Sarsat in 1996, which are associated with the pathogenesis of 
      atherosclerosis. However, the mechanisms by which AOPPs 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 
      AOPPs on MCP-1 expression in cultured vascular smooth muscle cells (VSMCs). 
      METHODS: VSMCs were cultured and then co-incubated with AOPP (200 micromol/L, 400 
      micromol/L) for different times with or without pretreatment with specific p38 
      mitogen-activated protein kinase (MAPK) inhibitor SB203580. RT-PCR and Western 
      blott were used to detect MCP-1 mRNA and protein expression at different time 
      points after AOPP stimulation in rat smooth muscle cells. Western blot was used 
      to detect the expression of phosphorylated p38 MAPK. RESULTS: Treatment of VSMC 
      with AOPPs resulted in a significant increase of the expression of MCP-1 mRNA and 
      protein in time- and dose-dependent manner, and could activated p38 MAPK. 
      Pretreatment of VSMCs with SB203580 resulted in a dose-dependent inhibition of 
      AOPPs-induced MCP-1 mRNA and protein expression. CONCLUSIONS: AOPPs can stimulate 
      MCP-1 expression via p38 MAPK in VSMCs. This suggests that AOPPs might contribute 
      to the formation of atherosclerosis through this proinflammatory effect.
FAU - Peng, Kan-fu
AU  - Peng KF
AD  - Department of Nephrology, Southwest Hospital, Third Military Medical University, 
      Chongqing 400038, China.
FAU - Wu, Xiong-fei
AU  - Wu XF
FAU - Zhao, Hong-wen
AU  - Zhao HW
FAU - Sun, Yan
AU  - Sun Y
LA  - eng
PT  - Journal Article
PL  - China
TA  - Chin Med J (Engl)
JT  - Chinese medical journal
JID - 7513795
RN  - 0 (Chemokine CCL2)
RN  - 0 (Imidazoles)
RN  - 0 (Proteins)
RN  - 0 (Pyridines)
RN  - 0 (RNA, Messenger)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - OU13V1EYWQ (SB 203580)
SB  - IM
MH  - Animals
MH  - Atherosclerosis/*etiology
MH  - Cardiovascular Diseases/etiology
MH  - Cells, Cultured
MH  - Chemokine CCL2/*genetics
MH  - Enzyme Activation
MH  - Imidazoles/pharmacology
MH  - Kidney Failure, Chronic/complications
MH  - Male
MH  - Muscle, Smooth, Vascular/cytology/*metabolism
MH  - Myocytes, Smooth Muscle/*metabolism
MH  - Oxidation-Reduction
MH  - Proteins/*metabolism
MH  - Pyridines/pharmacology
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Uremia/*metabolism
MH  - p38 Mitogen-Activated Protein Kinases/*physiology
EDAT- 2006/07/13 09:00
MHDA- 2006/08/10 09:00
CRDT- 2006/07/13 09:00
PHST- 2006/07/13 09:00 [pubmed]
PHST- 2006/08/10 09:00 [medline]
PHST- 2006/07/13 09:00 [entrez]
PST - ppublish
SO  - Chin Med J (Engl). 2006 Jul 5;119(13):1088-93.