Adrenomedullin suppresses interleukin-1β-induced tumor necrosis factor-α production in Swiss 3T3 cells

被引：66

作者：

Isumi, Y ^{[1
]}

Kubo, A ^{[1
]}

Katafuchi, T ^{[1
]}

Kangawa, K ^{[1
]}

Minamino, N ^{[1
]}

机构：

[1] Natl Cardiovasc Ctr, Res Inst, Osaka 5658565, Japan

来源：

FEBS LETTERS | 1999年 / 463卷 / 1-2期

基金：

日本科学技术振兴机构;

关键词：

adrenomedullin; tumor necrosis factor-alpha; interleukin-1; beta; fibroblast;

D O I：

10.1016/S0014-5793(99)01615-4

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

We demonstrated that adrenomedullin (AM) inhibited interleukin-1 beta-induced tumor necrosis factor-alpha (TNF-alpha) secretion and gene transcription in Swiss 3T3 fibroblasts maximally to 23% and 18% of control, while the other peptides elevating intracellular cAMP levels elicited much weaker effects. AM rapidly reduced the gene transcript level of TNF-alpha, inducing a maximal effect within 1 h, The inhibitory effect of AM was restored with an AM receptor antagonist as well as a cAMP-dependent protein kinase inhibitor, These findings indicate that AAI is a potent and quick suppressor of TNF-alpha production in Sn iss 3T3 cells acting through the cAMP protein kinase A pathway. As TNF-alpha is a major inflammatory cytokine and stimulates AM production in fibroblasts, AM is deduced to be an autocrine or paracrine factor suppressing inflammation through the inhibition of TNF-alpha production. (C) 1999 Federation of European Biochemical Societies.

引用

页码：110 / 114

页数：5

共 29 条

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