期刊
NEUROCHEMICAL RESEARCH
卷 48, 期 3, 页码 874-884出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-022-03812-9
关键词
Hypoxic-ischemic encephalopathy; HT22 cells; miR-19b-3p; SOX6; Wnt/beta-catenin pathway
This study found that miR-19b-3p expression was down-regulated and SOX6 expression was up-regulated in patients with hypoxic-ischemic encephalopathy (HIE). Overexpression of miR-19b-3p could alleviate HIE cell injury by inhibiting SOX6 expression and activating the Wnt/β-catenin pathway.
Hypoxic-ischemic encephalopathy (HIE) is a detrimental factor in infant death and chronic disease. The specific pathogenesis is not entirely clear. Therefore, exploring the pathogenesis of HIE is critical. The expression of miR-19b-3p and SOX6 in umbilical blood of HIE patients was detected by qRT-PCR assay. HT22 cells were triggered with oxygen-glucose deprivation/reoxygenation (OGD/R) to construct the HIE cell model. Cell Counting Kit-8 (CCK-8) assay was used to estimate viability. SOD and MDA levels were detected by enzyme linked immunosorbent assay. Flow cytometry was implemented to ascertain neurocyte apoptosis. Cellular beta-catenin immunofluorescence staining was used to detect the expression and distribution of beta-catenin protein. Wnt signaling pathway activation was detected by TOPFlash/FOPFlash luciferase reporter assay. The targeting correlation of SOX6 and miR-19b-3p was corroborated by dual-luciferase reporter gene assay and RNA pull-down assay. MiR-19b-3p expression was once down-regulated, whilst SOX6 expression was up-regulated in HIE patients. MiR-19b-3p overexpression promoted cell proliferation, repressed cell apoptosis, oxidative stress response, and Wnt/beta-catenin pathway activation in OGD/R-triggered HT22 cells. MiR-19b-3p negatively regulated SOX6 expression. SOX6 knockdown improved OGD/R-triggered HT22 cells injury via Wnt/beta-catenin pathway activation. MiR-19b-3p overexpression suppressed OGD/R-triggered HT22 cell injury via inhibiting SOX6 expression via activating Wnt/beta-catenin pathway.
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