Exercise-mediated IL-6 signaling occurs independent of inflammation and is amplified by training in mouse adipose tissue

Exercise-mediated IL-6 signaling occurs independent of inflammation and is amplified by training in mouse adipose tissue
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DOI:
10.1152/japplphysiol.00551.2015
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发表时间:
2015-12-01
影响因子:
3.3
通讯作者:
Wright, David C.
Wright, David C.
中科院分区:
医学2区
文献类型:
--
作者:
Castellani, Laura;Perry, Christopher G. R.;Wright, David C.

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这项研究的目的是确定运动诱导的脂肪组织白介素6(IL-6)信号的增加是否是运动引起的更大的促炎反应的一部分,以及在训练的小鼠中,急性运动引起的IL-6信号的诱导是否与IL-6受体复合体的变化平行地改变。对久坐不动、训练有素的C57BL/6J小鼠进行一次急性运动。分别于即刻和4h采集脂肪组织和血浆,分析IL-6信号、循环IL-6、脂肪组织炎症标志物、IL-6受体和糖蛋白130(Gp130)表达/含量的变化。非训练组小鼠运动后即刻IL-6mRNA表达增加,运动后4h附睾部IL-6信号转导指数增加,但腹股沟脂肪组织IL-6信号转导指数增加不明显。这与血浆IL-6的升高和炎症标志物的变化无关。与未训练的小鼠相比,在训练的小鼠中,急性运动诱导了gp130和IL-6受体α(IL-6Rα)的表达,并且训练增加了这些蛋白的含量。急性运动可诱导附睾糖蛋白130和IL-6Rα的表达,并使其蛋白质含量增加,且与训练后小鼠附睾部脂肪组织中IL-6信号转导标志物的增加有关。外源性IL-6促进STAT3磷酸化的能力在组间相似。我们的发现表明,急性运动以一种仓库依赖的方式增加IL-6信号,可能是通过自分泌/旁分泌机制。在训练过的小鼠中,这种反应在运动后启动得更快,可能是由于IL-6Rα和gp130增加的结果。
The purpose of this investigation was to determine whether exercise-induced increases in adipose tissue interleukin 6 (IL-6) signaling occurred as part of a larger proinflammatory response to exercise and whether the induction of IL-6 signaling with acute exercise was altered in trained mice in parallel with changes in the IL-6 receptor complex. Sedentary and trained C57BL/6J mice were challenged with an acute bout of exercise. Adipose tissue and plasma were collected immediately and 4 h afterward and analyzed for changes in indices of IL-6 signaling, circulating IL-6, markers of adipose tissue inflammation, and expression/content of IL-6 receptor and glycoprotein 130 (gp130). In untrained mice, IL-6 mRNA increased immediately after exercise, and increases in indices of IL-6 signaling were increased 4 h after exercise in epididymal, but not inguinal adipose tissue. This occurred independent of increases in plasma IL-6 and alterations in markers of inflammation. When compared with untrained mice, in trained mice, acute exercise induced the expression of gp130 and IL-6 receptor alpha (IL-6R alpha), and training increased the protein content of these. Acute exercise induced the expression, and training increased the protein content, of glycoprotein 130 and IL-6R alpha and was associated with a more rapid increase in markers of IL-6 signaling in epididymal adipose tissue from trained compared with untrained mice. The ability of exogenous IL-6 to increase phosphorylation of STAT3 was similar between groups. Our findings demonstrate that acute exercise increases IL-6 signaling in a depot-dependent manner, likely through an autocrine/paracrine mechanism. This response is initiated more rapidly after exercise in trained mice, potentially as a result of increases in IL-6R alpha and gp130.