Oncostatin M induces C2C12 myotube atrophy by modulating muscle differentiation and degradation.
Oncostatin M induces C2C12 myotube atrophy by modulating muscle differentiation and degradation.
复制标题
制瘤素 M 通过调节肌肉分化和降解来诱导 C2C12 肌管萎缩。
DOI：
10.1016/j.bbrc.2019.06.143
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发表时间：
2019
期刊：
影响因子：
--
通讯作者：
Inaba M.
中科院分区：
文献类型：
--
作者：
Miki Y;Morioka T;Shioi A;Fujimoto K;Sakura T;Uedono H;Kakutani Y;Ochi A;Mori K;Shoji T;Emoto M;Inaba M.
抑瘤素M（Oncostatin M，OSM）是白细胞介素-6家族的一种细胞因子，在各种疾病如癌症和炎性疾病中发挥作用，这些疾病通常伴有骨骼肌萎缩或肌肉减少症。然而，OSM在调节骨骼肌质量中的作用仍有待确定。本研究探讨了OSM对体外培养的C2 C12肌管形成的影响。将C2 C12成肌细胞诱导分化为肌管3d，然后用OSM处理24或48 h。OSM处理24和48 h后，分化的C2 C12肌管直径分别比对照组减少18.7%和23.3%。与对照细胞相比，OSM处理24 h的C2 C12肌管中MyoD和肌细胞生成素的表达水平降低，而atrogin-1、CCAAT/增强子结合蛋白δ和OSM受体的表达水平升高。此外，OSM对肌管形成的抑制作用显着减弱预处理与信号转导和转录激活因子（STAT）3的抑制剂或敲低Stat 3。最后，OSM诱导的MyoD、肌细胞生成素和atrogin-1表达水平的变化通过用STAT 3抑制剂预处理或通过C2 C12肌管中的Stat 3敲低而逆转。总之，OSM通过以STAT 3依赖性方式抑制肌源性分化和激活肌肉降解来诱导C2 C12肌管萎缩。
Oncostatin M (OSM) is a cytokine of the interleukin-6 family and plays a role in various disorders such as cancer and inflammatory diseases, which are often accompanied by skeletal muscle atrophy, or sarcopenia. However, the role of OSM in the regulation of skeletal muscle mass remains to be identified. In this study, we investigated the effect of OSM on C2C12 myotube formationin vitro. C2C12 myoblasts were induced to differentiate into myotubes for 3 days and then treated with OSM for 24 or 48 h. The diameter of differentiated C2C12 myotubes were reduced by 18.7% and 23.3% compared to control cells after treatment with OSM for 24 and 48 h, respectively. The expression levels of MyoD and myogenin were decreased, while those of atrogin-1, CCAAT/enhancer binding protein δ, and OSM receptor were increased in C2C12 myotubes treated with OSM for 24 h compared to control cells. Furthermore, the inhibitory effect of OSM on myotube formation was significantly attenuated by pretreatment with an inhibitor of signal transducer and activator of transcription (STAT) 3 or by knockdown ofStat3. Finally, the OSM-induced changes in the expression levels of MyoD, myogenin, and atrogin-1 were reversed by pretreatment with an inhibitor of STAT3 or byStat3knockdown in C2C12 myotubes. In conclusion, OSM induces C2C12 myotube atrophy by inhibiting myogenic differentiation and activating muscle degradation in a STAT3-dependent manner.
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