Signals through gp130 upregulate Wnt5a and contribute to cell adhesion in cardiac myocytes

被引：39

作者：

Fujio, Y

Matsuda, T

Oshima, Y

Maeda, M

Mohri, T

Ito, T

Takatani, T

Hirata, M

Nakaoka, Y

Kimura, R

Kishimoto, T

Azuma, J

机构：

[1] Grad Sch Pharmaceut Sci, Dept Clin Evaluat Med & Therapeut, Suita, Osaka 5650871, Japan

[2] Grad Sch Med Sci, Dept Mol Med, Osaka, Japan

[3] Osaka Univ, Grad Sch Frontier Sci, Lab Immune Regulat, Osaka, Japan

来源：

FEBS LETTERS | 2004年 / 573卷 / 1-3期

关键词：

IL-6; STAT3; Wnt; N-cadherin; cytokine; cardiomyocyte;

D O I：

10.1016/j.febslet.2004.07.082

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 [生物化学与分子生物学]; 081704 [应用化学];

摘要：

Glycoprotein 130 (gp130), a common receptor of IL-6 family cytokines, plays critical roles in cardiac functions. Here, we demonstrate that the stimulation of gp130 with leukemia inhibitory factor (LIF) promoted cell adhesion in a cadherin-dependent manner in cultured cardiomyocytes. Wnt5a was upregulated by the stimulation of gp130 with IL-6 family cytokines, accompanied by N-cadherin protein upregulation. Wnt5a was not induced by LIF in cardiomyocytes expressing dominant-negative STAT3. Ablation of Wnt5a by antisense cDNA inhibited LIF-induced cell adhesion. Collectively, signals through gp130 upregulate Wnt5a through STAT3, promoting the N-cadherin-mediated cell adhesion. (C) 2004 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

收藏

页码：202 / 206

页数：5

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