Induction of granulocyte colony-stimulating factor by globular adiponectin via the MEK-ERK pathway
Induction of granulocyte colony-stimulating factor by globular adiponectin via the MEK-ERK pathway
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DOI：
10.1016/j.mce.2008.05.002
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发表时间：
2008-09-24
影响因子：
4.1
通讯作者：
Yamashita, Yoshihisa
中科院分区：
文献类型：
--
作者：
Kamio, Noriaki;Akifusa, Sumio;Yamashita, Yoshihisa
脂联素是一种脂肪细胞来源的细胞因子，影响许多生理过程，包括免疫功能和炎症。我们研究了球状脂联素(GAD)是否影响小鼠巨噬细胞(RAW264细胞)中炎症相关基因的表达。DNA芯片分析表明，粒细胞集落刺激因子(G-CSF)在Gad刺激的RAW264细胞中的表达上调幅度最大。Gad诱导的G-CSF分泌呈时间和时间依赖性增加。MEK1/2抑制剂U0126和MEK1抑制剂PD98059可降低Gad诱导的G-CSF mRNA表达和G-CSF蛋白生成。GAD诱导RAW264细胞中MEK1/2和ERK1/2的磷酸化。此外，PD98059和U0126可显著降低Gad诱导的MEK1/2和ERK1/2的磷酸化水平。综上所述，这些结果提示MEK1/2-ERK1/2信号参与了脂联素诱导的G-CSF的分泌。(C)2008爱思唯尔爱尔兰有限公司。保留所有权利。
Adiponectin, an adipocyte-derived cytokine, affects a number of physiological processes, including immune function and inflammation. We investigated whether globular adiponectin (gAd) affects the expression of inflammation-related genes in murine macrophages (RAW264 cells). DNA microarray analysis indicated that granulocyte colony-stimulating factor (G-CSF) showed the largest increase in expression in gAd-stimulated RAW264 cells. The gAd-induced secretion of G-CSF increased in a time- and close-dependent manner. U0126 (MEK1/2 inhibitor) and PD98059 (MEK1 inhibitor) reduced the gAd-induced G-CSF mRNA expression and G-CSF Protein production. gAd induced the phosphorylation of MEK1/2 and ERK1/2 in RAW264 cells. In addition, the gAd-induced phosphorylation of MEK1/2 and ERK1/2 was dramatically reduced by PD98059 and U0126, respectively. Collectively, these results suggest that MEK1/2-ERK1/2 signaling is involved in the adiponectin-induced secretion of G-CSF. (C) 2008 Elsevier Ireland Ltd. All rights reserved.