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首页> 外文期刊>Experimental and clinical endocrinology and diabetes: Official journal, German Society of Endocrinology [and] German Diabetes Association >Interleukin-1 beta Increases Angptl4 (FIAF) Expression via the JNK Signaling Pathway in Osteoblastic MC3T3-E1 Cells
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Interleukin-1 beta Increases Angptl4 (FIAF) Expression via the JNK Signaling Pathway in Osteoblastic MC3T3-E1 Cells

机译:白细胞介素1 beta通过成骨细胞MC3T3-E1细胞的JNK信号通路增加Angptl4(FIAF)表达。

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Angiopoietin-like protein 4 (Angptl4), also known as fasting-induced adiopogenic factor (FIAF), has recently been reported to influence bone metabolism. However, there have been few studies on regulatory factors other than hypoxia for Angptl4 in bone, and particularly in osteoblasts. Expression of interleukin-1 beta (IL-1 beta), a proinflammatory cytokine, is increased in serum or bone microenvironments in inflammatory bone diseases or estrogen deficient-conditions. The present study was conducted to determine whether Angptl4 expression in osteoblasts is affected by IL-1 beta and investigate its involvement in MAP kinase signaling pathways. Angptl4 RNA levels were increased by IL-1 beta treatment in murine MC3T3-E1 osteoblastic cells. Western blotting and immunofluorescent staining showed a corresponding increase in Angptl4 protein. IL-1 beta treatment of osteoblasts induced phosphorylation of mitogen-activated protein kinases (MAPKs) including extracellular regulated kinases (ERKs), p38, and c-Jun N-terminal kinase (JNK). Furthermore, SP600125, an inhibitor of JNK, significantly blocked the upregulation of Angptl4 by IL-1 beta. In contrast, treatment with an inhibitor of p38 MAP kinase (SB203580) or an ERK inhibitor (PD98059) produced responses similar to those seen with the DMSO control. Taken together, these results suggest that IL-1 beta increases Angptl4 expression through a mechanism dependent on the JNK-MAPK signaling pathway in MC3T3-E1 cells.
机译:最近有报道称血管生成素样蛋白4(Angptl4)也被称为禁食诱导的脂肪形成因子(FIAF),可影响骨骼代谢。然而,除了缺氧的骨骼,尤其是成骨细胞中的Angptl4以外,很少有关于调节因子的研究。在炎症性骨疾病或雌激素缺乏症的血清或骨骼微环境中,促炎性细胞因子白介素-1β(IL-1 beta)的表达增加。进行本研究以确定成骨细胞中Angptl4表达是否受到IL-1 beta的影响,并调查其在MAP激酶信号通路中的参与。通过IL-1β处理,在鼠MC3T3-E1成骨细胞中Angptl4 RNA水平增加。 Western印迹和免疫荧光染色显示Angptl4蛋白相应增加。 IL-1β治疗成骨细胞可诱导丝裂原活化蛋白激酶(MAPK)磷酸化,包括细胞外调节激酶(ERK),p38和c-Jun N端激酶(JNK)。此外,JNK的抑制剂SP600125显着阻断了IL-1 beta对Angptl4的上调。相反,用p38 MAP激酶抑制剂(SB203580)或ERK抑制剂(PD98059)治疗产生的反应与DMSO对照所见相似。综上,这些结果表明,IL-1β通过依赖于MC3T3-E1细胞中JNK-MAPK信号传导途径的机制增加Angptl4表达。

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