MicroRNA-425-5p promotes tau phosphorylation and cell apoptosis in Alzheimer's disease by targeting heat shock protein B8

被引:26
|
作者
Yuan, Jiao [1 ]
Wu, Yanpeng [1 ]
Li, Lu [1 ]
Liu, Chuanqin [1 ]
机构
[1] Qingdao Mental Hlth Ctr, 299 Nanjing Rd, Qingdao 266000, Shandong, Peoples R China
关键词
MicroRNA-425-5p; AD; GSK-3; beta; HSPB8; Apoptosis; MISFOLDED PROTEINS; AUTOPHAGIC REMOVAL; AMYLOID-BETA; HSPB8;
D O I
10.1007/s00702-019-02134-5
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Alzheimer's disease (AD) is the most prevalent and age-related dementia accompanied by neurodegenerative disorder, memory loss, and abnormal behaviors. Recent studies have shown an increasing interest in studying the role of microRNAs (miRNAs) and their potential values in the early diagnostics of AD. MiR-425-5p has extensively expression within various tissues and organs, acting as an important regulator in many pathological procedures. The functions of miR-425-5p involved in AD were investigated in the present study. The results showed that miR-425-5p was upregulated in patients with AD and HEK293/tau cells. Transfections with miR-425-5p overexpression vector significantly enhanced cell apoptosis, activated glycogen synthase kinase-3 beta (GSK-3 beta), and increased tau phosphorylation in HEK293/tau cells. Heat shock protein B8 (HSPB8) was directly targeted by miR-425-5p. Upregulation of miR-425-5p induced cell apoptosis and promoted tau phosphorylation partially via targeting HSPB8 in AD. Therefore, miR-425-5p might act as a new therapeutic target for AD treatment.
引用
收藏
页码:339 / 346
页数:8
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