PMID- 19107603
OWN - NLM
STAT- MEDLINE
DCOM- 20090618
LR  - 20211020
IS  - 1355-008X (Print)
IS  - 1355-008X (Linking)
VI  - 35
IP  - 2
DP  - 2009 Apr
TI  - c-Jun N-terminal kinases inhibitor suppresses the TNF-alpha induced MCP-1 
      expression in human umbilical vein endothelial cells.
PG  - 184-8
LID - 10.1007/s12020-008-9136-0 [doi]
AB  - Monocyte chemoattractant protein-1 (MCP-1) is a 76-amino-acid chemokine that is 
      considered to be an important chemotactic factor for monocytes. MCP-1 is 
      expressed in the macrophage-rich areas of atherosclerotic lesions. A recent 
      report indicated that MCP-1 expression in human umbilical vein endothelial cells 
      (HUVECs) is induced by the stimulation of tumor necrosis factor (TNF)-alpha via 
      the c-Jun N-terminal kinases (JNK) pathway. In this study, we examined the 
      effects of JNK inhibitor (JNKI-1), on MCP-1 expression. The results of this study 
      indicated that the expression of MCP-1 mRNA and protein were stimulated in the 
      presence of TNF-alpha. TNF-alpha stimulated the phosphrylation of JNK, however, 
      JNKI-1 inhibited the TNF-alpha stimulated MCP-1 secretion and gene expression. As 
      expected, JNKI-1 blocked the stimulatory effect of TNF-alpha on the MCP-1 
      promoter activity. In conclusion, JNKI-1 partially inhibits the TNF-alpha-induced 
      MCP-1 expression in HUVECs, and therefore JNKI-1 may be of therapeutic value in 
      the treatment of diseases such as atherosclerosis.
FAU - Ahmed, Rania Abdel Muneem
AU  - Ahmed RA
AD  - Division of Endocrinology and Metabolism, Department of Internal Medicine, 
      Faculty of Medicine, Kagawa University, 1750-1 Ikenobe Miki-cho, Kita-gun, Kagawa 
      761-0793, Japan.
FAU - Murao, Koji
AU  - Murao K
FAU - Imachi, Hitomi
AU  - Imachi H
FAU - Yoshida, Kazuya
AU  - Yoshida K
FAU - Dobashi, Hiroaki
AU  - Dobashi H
FAU - Hosomi, Naohisa
AU  - Hosomi N
FAU - Ishida, Toshihiko
AU  - Ishida T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20081224
PL  - United States
TA  - Endocrine
JT  - Endocrine
JID - 9434444
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Cells, Cultured
MH  - Chemokine CCL2/*genetics
MH  - Endothelial Cells/*chemistry
MH  - Enzyme Inhibitors/*pharmacology
MH  - Gene Expression/drug effects
MH  - Humans
MH  - JNK Mitogen-Activated Protein Kinases/*antagonists & inhibitors/physiology
MH  - Phosphorylation
MH  - Polymerase Chain Reaction
MH  - Promoter Regions, Genetic/genetics
MH  - RNA, Messenger/analysis
MH  - Signal Transduction/physiology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - Umbilical Veins/*chemistry
EDAT- 2008/12/25 09:00
MHDA- 2009/06/19 09:00
CRDT- 2008/12/25 09:00
PHST- 2008/09/29 00:00 [received]
PHST- 2008/11/24 00:00 [accepted]
PHST- 2008/10/27 00:00 [revised]
PHST- 2008/12/25 09:00 [entrez]
PHST- 2008/12/25 09:00 [pubmed]
PHST- 2009/06/19 09:00 [medline]
AID - 10.1007/s12020-008-9136-0 [doi]
PST - ppublish
SO  - Endocrine. 2009 Apr;35(2):184-8. doi: 10.1007/s12020-008-9136-0. Epub 2008 Dec 
      24.