PMID- 12732205
OWN - NLM
STAT- MEDLINE
DCOM- 20030618
LR  - 20190612
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 305
IP  - 1
DP  - 2003 May 23
TI  - High glucose accelerates MCP-1 production via p38 MAPK in vascular endothelial 
      cells.
PG  - 122-8
AB  - In diabetes mellitus (DM), hyperglycemia causes cardiovascular lesions through 
      endothelial dysfunction. Monocyte chemoattractant protein-1 (MCP-1) is implicated 
      in the pathogenesis of cardiovascular lesions. By using human umbilical vein 
      endothelial cells, we investigated the effect of hyperglycemia on MCP-1 
      production and its signaling pathways. Chronic incubation with high glucose 
      increased mRNA expression and production rate of MCP-1 in a time (1-7 days)- and 
      concentration (10-35 mM)-dependent manner. Chronic exposure to high glucose 
      resulted in enhancement of generation of reactive oxygen species (ROS), as 
      determined by increasing level of 2,7-dichlorofluorescein (DCF), and subsequent 
      activation of p38 mitogen-activated protein kinase (MAPK). Neither c-Jun 
      NH(2)-terminal kinase nor extracellular signal-regulated kinase1/2 was affected. 
      SB203580 or FR167653, p38 MAPK specific inhibitors, completely suppressed MCP-1 
      expression. Catalase suppressed p38 MAPK phosphorylation and MCP-1 expression. 
      These results indicate that hyperglycemia can accelerate MCP-1 production through 
      the mechanism involving p38 MAPK, ROS-sensitive signaling pathway, in vascular 
      endothelial cells.
FAU - Takaishi, Hiroshi
AU  - Takaishi H
AD  - Department of Internal Medicine, Kobe University Graduate School of Medicine, 
      7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
FAU - Taniguchi, Takahiro
AU  - Taniguchi T
FAU - Takahashi, Akihiro
AU  - Takahashi A
FAU - Ishikawa, Yuichi
AU  - Ishikawa Y
FAU - Yokoyama, Mitsuhiro
AU  - Yokoyama M
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Antioxidants)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Reactive Oxygen Species)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Antioxidants/pharmacology
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Endothelium, Vascular/drug effects/*enzymology/*metabolism
MH  - Gene Expression Regulation/drug effects
MH  - Glucose/antagonists & inhibitors/*pharmacology
MH  - Hydrogen Peroxide/metabolism
MH  - Kinetics
MH  - MAP Kinase Signaling System
MH  - Mitogen-Activated Protein Kinases/*physiology
MH  - Reactive Oxygen Species/metabolism
MH  - Up-Regulation
MH  - p38 Mitogen-Activated Protein Kinases
EDAT- 2003/05/07 05:00
MHDA- 2003/06/19 05:00
CRDT- 2003/05/07 05:00
PHST- 2003/05/07 05:00 [pubmed]
PHST- 2003/06/19 05:00 [medline]
PHST- 2003/05/07 05:00 [entrez]
AID - S0006291X03007125 [pii]
AID - 10.1016/s0006-291x(03)00712-5 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2003 May 23;305(1):122-8. doi: 
      10.1016/s0006-291x(03)00712-5.