首页> 外文期刊>Scandinavian journal of immunology. >IL-17 induces expression of vascular cell adhesion molecule through signalling pathway of NF-κB, but not Akt1 and TAK1 in vascular smooth muscle cells
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IL-17 induces expression of vascular cell adhesion molecule through signalling pathway of NF-κB, but not Akt1 and TAK1 in vascular smooth muscle cells

机译:IL-17通过NF-κB的信号传导途径诱导血管细胞粘附分子的表达,但不诱导血管平滑肌细胞中的Akt1和TAK1的表达

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摘要

Interleukin-17 (IL-17) plays an important role in several autoimmune diseases. IL-17 can induce the expression of vascular cell adhesion molecule (VCAM-1) in aortic vascular smooth muscle cells (SMCs), which is important for the development of atherosclerosis. However, the signalling pathway of IL-17-induced VCAM-1 expression remains unclear. In this study, we reported that IL-17-induced expression of VCAM-1 in SMCs is dependent on NF-κB, but independent of Akt1 and TAK1. This is because knocking down Akt1 or TAK1 by siRNA did not reduce IL-17-induced activation of NF-κB and expression of VCAM-1, whereas knocking down NF-κB by siRNA markedly inhibited IL-17-mediated upregulation of VCAM-1 expression. In addition, IL-17-induced expression of VCAM-1 is partially dependent on activation of ERK1/2. Therefore, these signalling pathways of IL-17-mediated upregulation of VCAM-1 expression might be therapeutic targets for treatment of IL-17-mediated inflammation.
机译:白介素17(IL-17)在几种自身免疫性疾病中起重要作用。 IL-17可以诱导主动脉血管平滑肌细胞(SMCs)中血管细胞粘附分子(VCAM-1)的表达,这对动脉粥样硬化的发展至关重要。但是,IL-17诱导的VCAM-1表达的信号传导途径仍不清楚。在这项研究中,我们报道了IL-17诱导的SMC中VCAM-1的表达依赖于NF-κB,但独立于Akt1和TAK1。这是因为通过siRNA敲除Akt1或TAK1不会降低IL-17诱导的NF-κB激活和VCAM-1的表达,而通过siRNA敲除NF-κB则明显抑制了IL-17介导的VCAM-1上调。表达。此外,IL-17诱导的VCAM-1表达部分依赖于ERK1 / 2的激活。因此,这些IL-17介导的VCAM-1表达上调的信号通路可能是治疗IL-17介导的炎症的治疗靶标。

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