UCHL1 Regulates Lipid and Perilipin 2 Level in Skeletal Muscle.
UCHL1 Regulates Lipid and Perilipin 2 Level in Skeletal Muscle.
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DOI：
10.3389/fphys.2022.855193
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发表时间：
2022
影响因子：
4
通讯作者：
中科院分区：
文献类型：
--
作者：
泛素c端水解酶L1 （Ubiquitin C-terminal hydrolase L1, UCHL1）是一种原发现于神经元中的去泛素化酶。我们发现UCHL1在慢氧化骨骼肌中高表达，但其功能仍有待充分了解。在本研究中，我们观察到骨骼肌和C2C12肌管中的UCHL1蛋白水平分别在空腹或葡萄糖饥饿下下调。UCHL1的骨骼肌选择性敲除（smKO）导致骨骼肌脂质含量显著降低，葡萄糖耐量改善。UCHL1 smKO并没有显著改变参与氧化代谢的关键蛋白，如SDHA、Akt或PDH的水平。有趣的是，虽然主要脂肪酶和脂质转运蛋白的水平不变，但在UCHL1 smKO肌肉中，periilipin 2显著下调。与此一致的是，在C2C12肌管中，UCHL1 siRNA敲低也降低了perilipin 2蛋白水平。这一数据表明，UCHL1可以稳定periilipin 2，从而稳定骨骼肌中的脂质储存。
Ubiquitin C-terminal hydrolase L1 (UCHL1) is a deubiquitinating enzyme that was originally found in neurons. We found that UCHL1 is highly expressed in slow oxidative skeletal muscles, but its functions remain to be fully understood. In this study, we observed that UCHL1 protein levels in skeletal muscle and C2C12 myotubes were downregulated by fasting or glucose starvation respectively. Skeletal muscle selective knockout (smKO) of UCHL1 resulted in a significant reduction of lipid content in skeletal muscle and improved glucose tolerance. UCHL1 smKO did not significantly change the levels of key proteins involved in oxidative metabolism such as SDHA, Akt, or PDH. Interestingly, while the levels of the major lipases and lipid transporters were unchanged, perilipin 2 was significantly downregulated in UCHL1 smKO muscle. Consistently, in C2C12 myotubes, UCHL1 siRNA knockdown also reduced perilipin 2 protein level. This data suggests that UCHL1 may stabilize perilipin 2 and thus lipid storage in skeletal muscle.
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影响因子：
6.1
作者：
Gao, Hongbo;Freeling, Jessica;Li, Yifan
通讯作者：
Li, Yifan
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DOI：
10.1016/j.bbrc.2020.10.017
发表时间：
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影响因子：
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影响因子：
4.3
作者：
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影响因子：
6.5
作者：
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