Circulating inflammatory miRNA signature in response to different doses of aerobic exercise
Circulating inflammatory miRNA signature in response to different doses of aerobic exercise
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DOI：
10.1152/japplphysiol.00077.2015
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发表时间：
2015-07-15
影响因子：
3.3
通讯作者：
Iglesias-Gutierrez, Eduardo
中科院分区：
文献类型：
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作者：
de Gonzalo-Calvo, David;Davalos, Alberto;Iglesias-Gutierrez, Eduardo
虽然中度急性运动与强抗炎机制有关，但剧烈运动与有害的炎症扰动有关。因此，阐明调节运动诱导的炎症级联反应的机制是至关重要的。关于新型调节因子如循环炎性microRNA（c-inflammiRs）的信息是不完整的。在这项研究中，我们评估了一组c-炎性细胞对不同剂量的急性有氧运动的反应。我们首先研究了9名活跃的中年男性在10公里、半程马拉松和马拉松比赛之前和之后（0小时、24小时、72小时）的血清样本中运动诱导的炎症级联反应。接下来，我们分析了106种特异性c-炎性受体在10公里（低炎症反应）和马拉松（高炎症反应）比赛之前和之后（0小时，24小时）的循环概况。经典炎症参数分析显示有氧运动对全身炎症的剂量依赖性作用，马拉松后检测到更高的水平。我们观察到miR-150- 5 p在10公里比赛后立即增加。在马拉松后，12种c-炎性miR的水平立即增加（let-7 d-3 p、let-7 f-2- 3 p、miR-125 b-5 p、miR-132- 3 p、miR-143- 3 p、miR-148 a-3 p、miR-223- 3 p、miR-223- 5 p、miR-29 a-3 p、miR-34 a-5 p、miR-424- 3 p和miR-424- 5 p）。24小时后c-炎性受体恢复到基础水平。相关性和计算机模拟分析支持所观察到的c-炎性蛋白R模式与炎症过程的调节之间的密切关联。总之，我们发现，不同剂量的急性有氧运动诱导了一个独特的和特定的c-inflammamiR反应，这可能与运动诱导的炎症级联反应的控制。我们的研究结果指出，c-inflammiRs作为运动诱导的炎症的潜在生物标志物，因此，运动剂量。
While moderate acute exercise has been associated with strong anti-inflammatory mechanisms, strenuous exercise has been linked to deleterious inflammatory perturbations. It is therefore fundamental to elucidate the mechanisms that regulate the exercise-induced inflammatory cascade. Information on novel regulators such as circulating inflammatory microRNAs (c-inflammamiRs) is incomplete. In this study, we evaluated the response of a panel of c-inflammamiRs to different doses of acute aerobic exercise. We first studied the exercise-induced inflammatory cascade in serum samples of nine active middle-aged males immediately before and after (0 h, 24 h, 72 h) 10-km, half-marathon, and marathon races. Next, we analyzed the circulating profile of 106 specific c-inflammamiRs immediately before) and after (0 h, 24 h) 10-km (low inflammatory response) and marathon (high inflammatory response) races. Analysis of classical inflammatory parameters revealed a dose-dependent effect of aerobic exercise on systemic inflammation, with higher levels detected after marathon. We observed an increase in miR-150-5p immediately after the 10-km race. Levels of 12 c-inflammamiRs were increased immediately after the marathon (let-7d-3p, let-7f-2-3p, miR-125b-5p, miR-132-3p, miR-143-3p, miR-148a-3p, miR-223-3p, miR-223-5p, miR-29a-3p, miR-34a-5p, miR-424-3p, and miR-424-5p). c-inflammamiRs returned to basal levels after 24 h. Correlation and in silico analyses supported a close association between the observed c-inflammamiR pattern and regulation of the inflammatory process. In conclusion, we found that different doses of acute aerobic exercise induced a distinct and specific c-inflammamiR response, which may be associated with control of the exercise-induced inflammatory cascade. Our findings point to c-inflammamiRs as potential biomarkers of exercise-induced inflammation, and hence, exercise dose.