Fatigue-induced Orosomucoid 1 Acts on C-C Chemokine Receptor Type 5 to Enhance Muscle Endurance.
Fatigue-induced Orosomucoid 1 Acts on C-C Chemokine Receptor Type 5 to Enhance Muscle Endurance.
复制标题
疲劳诱导的 Orosumucoid 1 作用于 C-C 趋化因子受体 5 型以增强肌肉耐力
DOI：
10.1038/srep18839
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发表时间：
2016-01-07
影响因子：
4.6
通讯作者：
Liu X
中科院分区：
文献类型：
--
作者：
Lei H;Sun Y;Luo Z;Yourek G;Gui H;Yang Y;Su DF;Liu X
认识和处理疲劳是临床和社会面临的重大挑战。在试图探索身体对疲劳的反应和调节的过程中，我们在啮齿动物疲劳模型中发现，在包括血液和肌肉在内的多个组织中，orosomucid 1(ORM1)的表达显著增加。有趣的是，外源性ORM1可增加肌肉糖原，提高肌肉耐力，而在体内和体外，外源性ORM1缺乏都会导致肌肉耐力显著下降，这在很大程度上可以通过外源ORM1恢复。进一步的研究表明，ORM1可以与肌细胞上的C-C趋化因子受体5(CCR5)结合，该受体的缺失将阻断ORM1的作用。因此，疲劳上调了ORM1的水平，ORM1反过来作为一种抗疲劳蛋白，通过CCR5途径增强肌肉耐力。调节ORM1和CCR5信号的水平可能是一种新的疲劳管理策略。
Understanding and managing fatigue is a significant challenge in clinic and society. In attempting to explore how the body responds to and regulates fatigue, we found in rodent fatigue models that orosomucoid 1 (ORM1) was significantly increased in multiple tissues, including blood and muscle. Interestingly, administration of exogenous ORM1 increased muscle glycogen and enhanced muscle endurance, whereas ORM1 deficiency resulted in a significant decrease of muscle endurance both in vivo and in vitro, which could largely be restored by exogenous ORM1. Further studies demonstrated that ORM1 can bind to C-C chemokine receptor type 5 (CCR5) on muscle cells and deletion of the receptor abolished the effect of ORM1. Thus, fatigue upregulates the level of ORM1, which in turn functions as an anti-fatigue protein to enhance muscle endurance via the CCR5 pathway. Modulation of the level of ORM1 and CCR5 signaling could be a novel strategy for the management of fatigue.