期刊
CELL CYCLE
卷 20, 期 1, 页码 112-125出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2020.1863681
关键词
Alzheimer's disease; long non-coding RNA H19; MicroRNA-129; high mobility group box-1 protein; A beta(25-35); PC12 cells; apoptosis; viability
类别
资金
- Inner Mongolia Natural Science Foundation [2018MS08127]
- National Natural Science Foundation of China [81660720]
- Program for Young Talents of Science and Technology in Universities of Inner Mongolia Autonomous Region
Long non-coding RNA H19 and microRNA-129 are key players in the pathogenesis of Alzheimer's disease, regulating cell viability and apoptosis in response to A beta(25-35) stimulation. Modulation of these molecules may have therapeutic potential for Alzheimer's disease treatment.
Accumulating data manifest that long non-coding RNA (lncRNAs) are involved in all kinds of neurodegenerative disorders, consisting of the onset and progression of Alzheimer's disease (AD). The study was for the research of the mechanism of lncRNA H19 (H19) in viability and apoptosis of PC12 cells induced by A beta(25-35) in a cellular model of AD with the regulation of microRNA (miR)-129 and high mobility group box-1 protein (HMGB1). An AD cellular model of PC12 cells was established using A beta(25-35). The A beta(25-35)-induced PC12 cells were transfected with si-H19 or miR-129 mimic to figure their roles in cell viability,apoptosis, mitochondrial membrane potential dysfunction and oxidative stress in AD. Luciferase reporter assay and RNA-pull down assay were employed for verification of the binding relationship between H19 and miR-129 and the targeting relationship between miR-129 and HMGB1. An AD mouse model was induced and brain tissues were collected. H19, miR-129 and HMGB1 were detected in A beta(25-35)-treated cells and brain tissues of AD mice. Elevated H19, HMGB1 and decreased miR-129 were found in A beta(25-35)-treated PC12 cells as well as in brain tissues of AD mice. Silenced H19 or elevated miR-129 promoted viability, inhibited apoptosis, prevented mitochondrial membrane potential dysfunction and decreased oxidative stress in A beta(25-35)-treated PC12 cells. H19 could specifically bind to miR-129. MiR-129 specifically suppressed HMGB1 expression. This study suggests that silenced H19 and up-regulated miR-129 accelerates viability and represses apoptosis of PC12 cells stimulated by A beta(25-35) in AD, which is beneficial for AD treatment.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据