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白细胞介素-6 上调人角质形成细胞系 HaCaT 中白细胞介素-15 的表达,与 MAPKs 和 PI3-K 信号通路有关。

Interleukin-6 up-regulates the expression of interleukin-15 is associated with MAPKs and PI3-K signaling pathways in the human keratinocyte cell line, HaCaT.

机构信息

Department of Biochemistry and Molecular Biology, Anhui Medical University, 69 Meishan Road, Hefei, 230032, Anhui, China.

出版信息

Mol Biol Rep. 2012 Apr;39(4):4201-5. doi: 10.1007/s11033-011-1205-4. Epub 2011 Jul 17.

DOI:10.1007/s11033-011-1205-4
PMID:21769475
Abstract

Interleukin (IL)-15 is an important inflammatory cytokine and plays a key role in autoimmune disease. At present, IL-15 gene expression and regulation related to many innate immunity trigger signals have been clarified in some specific cell types, but the relationship of IL-6 and IL-15 in the human keratinocyte cell line (HaCaT) is unknown. In this study, we investigated the effect of IL-6 on the expression of IL-15 and selected signaling pathways in HaCaT cells. Results demonstrated that IL-6 up-regulated the expression of IL-15 both at the mRNA and protein levels. Meanwhile, IL-6 was able to activate MAPKs-ERK1/2 and PI3K-AKT signaling pathways. Furthermore, the high expression of IL-15 induced by IL-6 was down-regulated while MAPKs-ERK1/2 and PI3K-AKT signaling pathways were, respectively, blocked by PD98059 and LY294002. These findings indicate that the expression of IL-15 up-regulated by IL-6 is associated with MAPKs-ERK1/2 and PI3K-AKT signaling pathways in HaCaT cells.

摘要

白细胞介素 (IL)-15 是一种重要的炎症细胞因子,在自身免疫性疾病中发挥关键作用。目前,在某些特定的细胞类型中,已经阐明了与许多先天免疫触发信号相关的 IL-15 基因表达和调节,但人角质形成细胞系 (HaCaT) 中 IL-6 和 IL-15 之间的关系尚不清楚。在本研究中,我们研究了 IL-6 对 HaCaT 细胞中 IL-15 表达和选择信号通路的影响。结果表明,IL-6 可在上、下调 IL-15 的 mRNA 和蛋白水平。同时,IL-6 能够激活 MAPKs-ERK1/2 和 PI3K-AKT 信号通路。此外,由 IL-6 诱导的 IL-15 高表达被 PD98059 和 LY294002 分别阻断 MAPKs-ERK1/2 和 PI3K-AKT 信号通路后下调。这些发现表明,IL-6 上调的 IL-15 表达与 HaCaT 细胞中的 MAPKs-ERK1/2 和 PI3K-AKT 信号通路有关。

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Association of IL-6 promoter and IFN-γ gene polymorphisms with acute rejection of liver transplantation.白细胞介素-6 启动子和干扰素-γ 基因多态性与肝移植急性排斥反应的关系。
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Interleukin-6⁻¹⁷⁴ and tumor necrosis factor α⁻³⁰⁸ polymorphisms enhance cytokine production by human macrophages exposed to respiratory viruses.
软脂酸游离脂肪酸损害培养的人膀胱平滑肌细胞的活力和功能。
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白细胞介素-6⁻¹⁷⁴ 和肿瘤坏死因子 α⁻³⁰⁸ 多态性增强人类巨噬细胞暴露于呼吸道病毒后细胞因子的产生。
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