PMID- 10802155
OWN - NLM
STAT- MEDLINE
DCOM- 20000719
LR  - 20190910
IS  - 0168-8227 (Print)
IS  - 0168-8227 (Linking)
VI  - 48
IP  - 3
DP  - 2000 Jun
TI  - Inhibitory effect of troglitazone on TNF-alpha-induced expression of monocyte 
      chemoattractant protein-1 (MCP-1) in human endothelial cells.
PG  - 171-6
AB  - Insulin resistance is one of the risk factors for the progression of 
      atherosclerosis. Recently, the new oral insulin-sensitizing drug troglitazone is 
      thought to offer potential in the treatment of diabetes. If adopted for such use, 
      this drug might be helpful in protecting against the development of 
      atherosclerosis and microvascular complications via its improvement of insulin 
      resistance. However, it has not yet been clarified whether troglitazone acts 
      directly on the vascular cells and inhibits the progression of atherosclerosis. 
      Meanwhile, Monocyte chemoattractant protein-1 (MCP-1) is known to play an 
      important role in the pathogenesis of atherosclerosis by inducing monocyte 
      migration. Therefore, we investigated the effect of troglitazone on the 
      expression of MCP-1 in human umbilical vein endothelial cells (HUVECs). HUVECs 
      were treated with or without troglitazone (1 or 10 microM) in the presence or 
      absence of various concentrations of tumor necrosis factor-alpha (TNF-alpha) (5, 
      50 or 500 ng/ml), and then the amounts of MCP-1 secreted from the HUVECs were 
      measured. We found that TNF-alpha increased the secretions of MCP-1 119-fold vs. 
      control, and that troglitazone significantly inhibited this TNF-alpha-induced 
      increase in MCP-1 secretions (19.4%). Moreover, Northern blot analysis revealed 
      that troglitazone decreased the MCP-1 mRNA level in HUVECs. Our present studies 
      indicated that troglitazone may prevent the progression of atherosclerosis by 
      inhibiting MCP-1 expression in endothelial cells.
FAU - Ohta, M Y
AU  - Ohta MY
AD  - First Department of Internal Medicine, School of Medicine, Kanazawa University, 
      13-1 Takara-machi, Kanazawa, Ishikawa, Japan.
FAU - Nagai, Y
AU  - Nagai Y
FAU - Takamura, T
AU  - Takamura T
FAU - Nohara, E
AU  - Nohara E
FAU - Kobayashi, K
AU  - Kobayashi K
LA  - eng
PT  - Journal Article
PL  - Ireland
TA  - Diabetes Res Clin Pract
JT  - Diabetes research and clinical practice
JID - 8508335
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chromans)
RN  - 0 (RNA, Messenger)
RN  - 0 (Thiazoles)
RN  - 0 (Thiazolidinediones)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - I66ZZ0ZN0E (Troglitazone)
SB  - IM
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Chromans/*pharmacology
MH  - Endothelium, Vascular/cytology/drug effects/*metabolism
MH  - Humans
MH  - RNA, Messenger/metabolism
MH  - Thiazoles/*pharmacology
MH  - *Thiazolidinediones
MH  - Troglitazone
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - Umbilical Veins/cytology/drug effects/metabolism
EDAT- 2000/05/10 09:00
MHDA- 2000/07/25 11:00
CRDT- 2000/05/10 09:00
PHST- 2000/05/10 09:00 [pubmed]
PHST- 2000/07/25 11:00 [medline]
PHST- 2000/05/10 09:00 [entrez]
AID - S0168822700001285 [pii]
AID - 10.1016/s0168-8227(00)00128-5 [doi]
PST - ppublish
SO  - Diabetes Res Clin Pract. 2000 Jun;48(3):171-6. doi: 
      10.1016/s0168-8227(00)00128-5.