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Signals through gp130 upregulate Wnt5a and contribute to cell adhesion in cardiac myocytes
Author(s) -
Fujio Yasushi,
Matsuda Takahisa,
Oshima Yuichi,
Maeda Makiko,
Mohri Tomomi,
Ito Takashi,
Takatani Tomoka,
Hirata Mayo,
Nakaoka Yoshikazu,
Kimura Ryusuke,
Kishimoto Tadamitsu,
Azuma Junichi
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.07.082
Subject(s) - downregulation and upregulation , glycoprotein 130 , leukemia inhibitory factor , microbiology and biotechnology , cell adhesion , chemistry , adhesion , cadherin , wnt5a , stat3 , cell , biology , signal transduction , cytokine , interleukin 6 , immunology , wnt signaling pathway , biochemistry , gene , organic chemistry
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.