PMID- 9222645
OWN - NLM
STAT- MEDLINE
DCOM- 19970916
LR  - 20131121
IS  - 0012-186X (Print)
IS  - 0012-186X (Linking)
VI  - 40
IP  - 6
DP  - 1997 Jun
TI  - Oxidized lipoproteins found in patients with NIDDM stimulate radical-induced 
      monocyte chemoattractant protein-1 mRNA expression in cultured human endothelial 
      cells.
PG  - 662-70
AB  - Although oxidized low density lipoprotein (LDL) exists in plasma from diabetic 
      patients, there are few studies on its biological activity. Thus, we investigated 
      the biological potency of LDL plus intermediate density lipoprotein fraction 
      isolated from 12 non-diabetic and 24 non-insulin-dependent diabetic subjects of 
      similar age and body mass index, in order to induce monocyte chemoattractant 
      protein-1 (MCP-1) mRNA expression in cultured human endothelial cells. MCP-1 mRNA 
      content in the cells exposed to the lipoproteins isolated from the diabetic 
      patients was significantly higher than that from the control subjects (p < 
      0.001). The increment of MCP-1 mRNA content was positively correlated with not 
      only HbA1c (r = 0.58, p < 0.0001) but also lysophosphatidylcholine (LPC) content 
      in the lipoprotein (r = 0.46, p < 0.005) and was negatively correlated with diene 
      formation lag time as a marker of oxidizability of the lipoprotein (r = -0.33, p 
      < 0.05). Treatments of the cells with either 50 mumol/l probucol, 50 mumol/l 
      alpha-tocopherol, or 0.1 mmol/l deferoxamine suppressed the increase in MCP-1 
      mRNA content induced by diabetic lipoproteins, respectively. Furthermore, the 
      diabetic lipoproteins activated nuclear transcription factor NF-kappa B in the 
      cells, which was inhibited by pre-treatment of cells with 50 mumol/l probucol. 
      These data indicate that oxidatively modified lipoproteins found in diabetic 
      plasma stimulate MCP-1 gene expression in endothelial cells. The LPC content 
      which reflects oxidative modification of lipoprotein is at least a possible 
      marker of biological activity to increase an atherogenic cytokine in endothelial 
      cells.
FAU - Takahara, N
AU  - Takahara N
AD  - Third Department of Medicine, Shiga University of Medical Science, Japan.
FAU - Kashiwagi, A
AU  - Kashiwagi A
FAU - Nishio, Y
AU  - Nishio Y
FAU - Harada, N
AU  - Harada N
FAU - Kojima, H
AU  - Kojima H
FAU - Maegawa, H
AU  - Maegawa H
FAU - Hidaka, H
AU  - Hidaka H
FAU - Kikkawa, R
AU  - Kikkawa R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Diabetologia
JT  - Diabetologia
JID - 0006777
RN  - 0 (Antioxidants)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lipoproteins)
RN  - 0 (RNA, Messenger)
RN  - 1406-18-4 (Vitamin E)
RN  - J06Y7MXW4D (Deferoxamine)
RN  - P3CTH044XJ (Probucol)
SB  - IM
MH  - Antioxidants/pharmacology
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis
MH  - Deferoxamine/pharmacology
MH  - Diabetes Mellitus, Type 2/*blood
MH  - Endothelium, Vascular/drug effects/*metabolism
MH  - Female
MH  - Humans
MH  - Lipoproteins/*blood/isolation & purification/*pharmacology
MH  - Male
MH  - Middle Aged
MH  - Oxidation-Reduction
MH  - Probucol/pharmacology
MH  - RNA, Messenger/biosynthesis
MH  - Reference Values
MH  - Regression Analysis
MH  - *Transcription, Genetic/drug effects
MH  - Umbilical Veins
MH  - Vitamin E/pharmacology
EDAT- 1997/06/01 00:00
MHDA- 1997/06/01 00:01
CRDT- 1997/06/01 00:00
PHST- 1997/06/01 00:00 [pubmed]
PHST- 1997/06/01 00:01 [medline]
PHST- 1997/06/01 00:00 [entrez]
AID - 10.1007/s001250050731 [doi]
PST - ppublish
SO  - Diabetologia. 1997 Jun;40(6):662-70. doi: 10.1007/s001250050731.