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首页> 外文期刊>Journal of Cellular Physiology >Interleukin 11 signaling in 3T3-L1 adipocytes.
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Interleukin 11 signaling in 3T3-L1 adipocytes.

机译：3 t3-l1脂肪细胞白介素11信号。

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摘要

Interleukin 11 (IL-11) is an anti-inflammatory cytokine with receptors located on most cell types and tissues throughout the body. Its anti-inflammatory properties are mediated through suppression of cytokine synthesis, in large part by prevention of NF-kappaB activation. As adipose tissue synthesizes and secretes cytokines involved in establishing insulin resistance and due to the ability of IL-11 to suppress cytokine synthesis, we initiated an investigation to determine the signal transduction pathways initiated by IL-11 in adipose tissue. Using the 3T3-L1 adipocyte cell culture model we demonstrate the rapid activation of the p44/42MAP kinase, PI3-kinase, and STATs 1 and 3. Activation of MAP kinase is demonstrated to lead to the downstream activation of p90 RSK (ribosomal S6 kinase) as well as ATF-1 and CREB. PI3-kinase appears to activate the downstream target of p70 S6 kinase resulting in phosphorylation of ribosomal protein S6. STAT phosphorylation appears to be initiated through PI3-kinase and to a lesser degree through p44/42 MAP kinase. These studies demonstrate the activation of three major signaling pathways and support a role for IL-11 in the regulation of both transcription and protein synthesis in fully differentiated adipocytes.
机译：白介素11 (IL-11)是一种抗炎细胞因子与受体位于大多数细胞类型和人体组织。抗炎作用是通过介导的抑制细胞因子的合成,在很大程度上通过预防NF-kappaB激活。组织合成和分泌细胞因子参与建立胰岛素抵抗由于IL-11抑制细胞因子的能力合成,我们发起了一个调查确定信号转导途径由IL-11在脂肪组织中。我们3 t3-l1脂肪细胞细胞培养模型演示p44/42MAP快速激活的pi3激酶激酶,统计1和3。导致显示MAP激酶激活下游p90 RSK(核糖体S6激酶)以及ATF-1和分子。似乎激活下游p70的目标S6激酶的磷酸化核糖体蛋白S6。似乎通过pi3激酶和启动一个较小的程度上通过p44/42 MAP激酶。研究表明三个主要的激活信号通路和支持IL-11的角色在转录和监管蛋白质合成的完全分化脂肪细胞。

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