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MKK4 is a novel target for the inhibition of tumor necrosis factor-alpha-induced vascular endothelial growth factor expression by myricetin.

Abstract：

:Tumor necrosis factor-alpha (TNF-alpha) is a mediator of multiple inflammatory diseases. Vascular endothelial growth factor (VEGF) plays a critical role in TNF-alpha-mediated diseases. We investigated the inhibitory effects of 3,3',4',5,5',7-hexahydroxyflavone (myricetin), an abundant natural flavonoid, on TNF-alpha-induced VEGF upregulation and the underlying molecular mechanism. Myricetin is a direct inhibitor of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) kinase 1 (MEK1) and inhibits neoplastic cell transformation. We found that myricetin inhibited TNF-alpha-induced VEGF expression in JB6 P+ mouse epidermal cells by targeting MAPK kinase 4 (MKK4), as well as MEK1. The activation of activator protein-1 by TNF-alpha was inhibited by myricetin in a dose-dependent manner. The phosphorylation of c-Jun N-terminal kinase (JNK) and ERK was inhibited by myricetin, but not the phosphorylation of their upstream kinases MKK4 and MEK1. TNF-alpha-induced VEGF expression was inhibited by SP600125 and U0126, which are inhibitors of JNK and MEK, respectively. Myricetin inhibited TNF-alpha-induced MKK4 activity and bound glutathione S-transferase-MKK4 directly by competing with ATP. Computer modeling suggested that myricetin docks onto the ATP-binding site in MKK4, which is located between the N- and C-lobes of the kinase domain. Overall, our results indicate that myricetin has potent chemopreventive effects against TNF-alpha-related disease, mainly by targeting MKK4 and MEK1.

journal_name

Biochem Pharmacol

journal_title

Biochemical pharmacology

authors

Kim JE,Kwon JY,Lee DE,Kang NJ,Heo YS,Lee KW,Lee HJ

doi

10.1016/j.bcp.2008.10.027

subject

Has Abstract

pub_date

2009-02-01 00:00:00

pages

412-21

issue

3

eissn

0006-2952

issn

1873-2968

pii

S0006-2952(08)00781-8

journal_volume

77

pub_type

杂志文章

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