Signals through gp130 upregulate Wnt5a and contribute to cell adhesion in cardiac myocytes
Signals through gp130 upregulate Wnt5a and contribute to cell adhesion in cardiac myocytes
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DOI：
10.1016/j.febslet.2004.07.082
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发表时间：
2004-08-27
期刊：
影响因子：
3.5
通讯作者：
Azuma, J
中科院分区：
文献类型：
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作者：
Fujio, Y;Matsuda, T;Azuma, J
糖蛋白130（Glycoprotein 130，gp 130）是IL-6家族细胞因子的共同受体，在心脏功能中起重要作用。在这里，我们表明，刺激gp 130与白血病抑制因子（LIF）促进细胞粘附在培养的心肌细胞中的钙粘蛋白依赖的方式。Wnt 5a通过用IL-6家族细胞因子刺激gp 130而上调，伴随着N-钙粘蛋白蛋白上调。在表达显性负性STAT 3的心肌细胞中，LIF不诱导Wnt 5a。反义cDNA阻断Wnt 5a抑制LIF诱导的细胞粘附。总的来说，通过gp 130的信号通过STAT 3上调Wnt 5a，促进N-钙粘蛋白介导的细胞粘附。(C)2004年欧洲生物化学学会联合会。Elsevier B. V.出版，保留所有权利。
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.