MiR-204 promotes apoptosis in oxidative stress-induced rat Schwann cells by suppressing neuritin expression
文献类型： 外文期刊
作者： Gao, Rui 1 ; Wang, Liming 3 ; Sun, Jun 1 ; Nie, Kun 2 ; Jian, Huiling 2 ; Gao, Lei 3 ; Liao, Xinhua 2 ; Zhang, Haiyuan 1 ; H 1 ;
作者机构： 1.Huazhong Univ Sci & Technol, Tongji Med Coll, Dept Biochem & Mol Biol, Wuhan 430030, Peoples R China
2.Shihezi Univ, Sch Med, Dept Basic Med Sci, Shihezi 832000, Peoples R China
3.Xinjiang Acad Agr & Reclamat Sci, Key Labs Sheep Breeding & Reproduce, Shihezi 832000, Peoples R China
4.Xinjiang Acad Agr & Reclamat
关键词： javax.sql.rowset.serial.SerialClob@4df3c1
期刊名称：FEBS LETTERS （ 影响因子：4.124； 五年影响因子：3.814 ）
ISSN：
年卷期：
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收录情况： SCI
摘要： Neuritin (Nrn1) is a neurotrophin that plays an important role in nervous system plasticity and repair following nerve injury. MicroRNAs (miRNAs) are a type of small non-coding RNA that regulate nearly all aspects of nerve development and survival, including apoptosis. Here it was found that miR-204 negatively regulates Nrn1 protein expression through direct interaction with Nrn1 transcript. Moreover, miR-204 activates cleaved caspase-3, enhancing the sensitivity of RSC96 Schwann cells to H2O2-induced oxidative stress and apoptosis. Thus, miR-204 expressed at a low level may create a microenvironment suitable for the repair of injured nerves by relieving the inhibition of Nrn1 transcription and stimulating the anti-apoptotic function of Schwann cells. These results provide novel insights into the roles of miR-204 in nerve injury and repair.
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