c-Jun N-terminal kinases inhibitor suppresses the TNF-α induced MCP-1 expression in human umbilical vein endothelial cells

被引：13

作者：

Ahmed, Rania Abdel Muneem ^{[1
]}

Murao, Koji ^{[1
]}

Imachi, Hitomi ^{[1
]}

Yoshida, Kazuya ^{[1
]}

Dobashi, Hiroaki ^{[1
]}

Hosomi, Naohisa ^{[2
]}

Ishida, Toshihiko ^{[1
]}

机构：

[1] Kagawa Univ, Div Endocrinol & Metab, Dept Internal Med, Fac Med, Miki, Kagawa 7610793, Japan

[2] Kagawa Univ, Dept Cardiorenal & Cerebrovasc Med, Fac Med, Miki, Kagawa 7610793, Japan

来源：

ENDOCRINE | 2009年 / 35卷 / 02期

关键词：

JNKI-1; MCP-1; TNF-alpha; JNK; HUVEC; MONOCYTE CHEMOATTRACTANT PROTEIN-1; SIGNAL-TRANSDUCTION PATHWAY; KAPPA B ACTIVATION; RECEPTOR CLASS BI; GENE-EXPRESSION; JNK; CHEMOKINES; ATHEROSCLEROSIS; STIMULATION; PEPTIDE;

D O I：

10.1007/s12020-008-9136-0

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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.

引用

页码：184 / 188

页数：5

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