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经动脉化疗栓塞术释放的肿瘤坏死因子-α介导机械转导诱导的p38丝裂原活化蛋白激酶激活和成肌作用。

TACE release of TNF-alpha mediates mechanotransduction-induced activation of p38 MAPK and myogenesis.

作者信息

Zhan Mei, Jin Bingwen, Chen Shuen-Ei, Reecy James M, Li Yi-Ping

机构信息

Department of Medicine, Baylor College of Medicine, One Baylor Plaza-520B, Houston, TX 77030, USA.

出版信息

J Cell Sci. 2007 Feb 15;120(Pt 4):692-701. doi: 10.1242/jcs.03372. Epub 2007 Jan 30.

DOI:10.1242/jcs.03372
PMID:17264149
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3099537/
Abstract

Skeletal muscle responds to mechanical stimulation by activating p38 MAPK, a key signal for myogenesis. However, the mechanotransduction mechanism that activates p38 is unknown. Here we show that mechanical stimulation of myoblasts activates p38 and myogenesis through stimulating TNF-alpha release by TNF-alpha converting enzyme (TACE). In C2C12 or mouse primary myoblasts cultured in growth medium, static stretch activated p38 along with ERK1/2, JNK and AKT. Disrupting TNF-alpha signaling by TNF-alpha-neutralizing antibody or knocking out TNF-alpha receptors blocked stretch activation of p38, but not ERK1/2, JNK or AKT. Stretch also activated differentiation markers MEF2C, myogenin, p21 and myosin heavy chain in a TNF-alpha- and p38-dependent manner. Stretch stimulated the cleavage activity of TACE. Conversely, TACE inhibitor TAPI or TACE siRNA abolished stretch activation of p38. In addition, conditioned medium from stretched myoblast cultures activated p38 in unstretched myoblasts, which required TACE activity in the donor myoblasts, and TNF-alpha receptors in the recipient myoblasts. These results indicate that posttranscriptional activation of TACE mediates the mechanotransduction that activates p38-dependent myogenesis via the release of TNF-alpha.

摘要

骨骼肌通过激活p38丝裂原活化蛋白激酶（p38 MAPK）对机械刺激做出反应，p38 MAPK是肌生成的关键信号。然而，激活p38的机械转导机制尚不清楚。在此我们表明，对成肌细胞的机械刺激通过肿瘤坏死因子-α转换酶（TACE）刺激肿瘤坏死因子-α（TNF-α）释放，从而激活p38和肌生成。在生长培养基中培养的C2C12或小鼠原代成肌细胞中，静态拉伸激活了p38以及细胞外信号调节激酶1/2（ERK1/2）、应激活化蛋白激酶（JNK）和蛋白激酶B（AKT）。用TNF-α中和抗体破坏TNF-α信号或敲除TNF-α受体可阻断p38的拉伸激活，但不影响ERK1/2、JNK或AKT。拉伸还以TNF-α和p38依赖的方式激活分化标志物肌细胞增强因子2C（MEF2C）、肌细胞生成素、p21和肌球蛋白重链。拉伸刺激了TACE的切割活性。相反，TACE抑制剂TAPI或TACE小干扰RNA（siRNA）消除了p38的拉伸激活。此外，来自拉伸的成肌细胞培养物的条件培养基激活了未拉伸的成肌细胞中的p38，这需要供体成肌细胞中的TACE活性以及受体成肌细胞中的TNF-α受体。这些结果表明，TACE的转录后激活介导了通过TNF-α释放激活p38依赖性肌生成的机械转导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/153a/3099537/72988e32b0e0/nihms226371f9.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/153a/3099537/72988e32b0e0/nihms226371f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/153a/3099537/1d8d363590eb/nihms226371f1.jpg
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