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Silencing of long noncoding RNA XIST attenuated Alzheimer's disease‐related BACE1 alteration through miR‐124
Author(s) -
Yue Du,
Guanqun Gao,
Jingxin Li,
Sen Suo,
Shuang Liu,
Yan Sun,
Minxue Zhang,
Ping Yin,
Chong Lu,
Zhuobo Zhang,
Yafen Wei
Publication year - 2020
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11263
Subject(s) - xist , gene silencing , long non coding rna , biology , rna interference , rna , microbiology and biotechnology , microrna , rna silencing , cancer research , genetics , gene , x inactivation , x chromosome
Alzheimer's disease (AD) is a chronic progressive neurodegenerative disorder. However, its pathogenetic mechanism is still poorly understood. An increasing number of studies have evidenced the important role of long noncoding RNAs (lncRNAs) in AD. The aim of the current study was to investigate the effect and molecular mechanism of the lncRNA X‐inactive specific transcript (XIST) in AD. Bilateral common carotid artery occlusion (2VO) was used to induce an AD model in mice. Hydrogen peroxide (H 2 O 2 ) was used to induce an AD model in N2a cells. The lncRNA XIST, miR‐124, and BACE1 messenger RNA expression levels were detected by a real‐time polymerase chain reaction. The BACE1 protein expression level was detected by western blot and immunofluorescence assay. The Aβ 1–42 expression level was detected using an enzyme‐linked immunosorbent assay kit. The expression level of lncRNA XIST was significantly upregulated in AD models, both in vivo and in vitro. Silencing of lncRNA XIST negatively regulated miR‐124 and positively regulated BACE1 expression in N2a cells, which is attenuated by cotransfection of anti‐miR‐124 oligodeoxyribonucleotide (AMO‐124). Silencing of lncRNA XIST reversed the effect of H 2 O 2 on miR‐124, BACE1, and Aβ 1–42 expression in N2a cells, which was reversed by cotransfection of AMO‐124. Silencing of lncRNA XIST attenuated AD‐related BACE1 alteration through miR‐124. LncRNA XIST may be a new potential target for the treatment of AD.