自噬
下调和上调
细胞凋亡
生物
细胞生物学
转染
磷酸化
小RNA
癌症研究
核心
NF-κB
CXCR4型
体外
细胞培养
免疫学
基因
生物化学
炎症
遗传学
趋化因子
作者
Zhongjie Sun,Xiaoming Tang,Haibin Wang,Hongzhi Sun,Peilin Chu,Liang Sun,Jie Tian
出处
期刊:Stem Cells and Development
[Mary Ann Liebert]
日期:2021-07-15
卷期号:30 (14): 736-748
被引量:19
标识
DOI:10.1089/scd.2021.0009
摘要
The etiology of lumbocrural pain is closely related to intervertebral disc degeneration (IDD). Long noncoding RNAs (lncRNAs) serve crucial roles in IDD progression. This study investigated the effect of lncRNA H19 on autophagy and apoptosis of nucleus pulposus cells (NPCs) in IDD. The rat model of IDD was established. Normal NPCs and degenerative NPCs (DNPCs) were cultured in vitro. H19 expression in IDD rat was detected. DNPCs were treated with si-H19 to evaluate autophagy and apoptosis of DNPCs. The binding relationships between H19 and miR-139-3p, and miR-139-3p and CXCR4 were verified. DNPCs were co-transfected si-H19 and miR-139-3p inhibitor. The phosphorylation of NF-κB pathway-related p65 in DNPCs was detected. LncRNA H19 was upregulated in IDD rats. Downregulation of H19 inhibited autophagy and apoptosis of DNPCs. LncRNA H19 sponged miR-139-3p to inhibit CXCR4 expression. si-H19 and miR-139-3p inhibitor co-treatment induced autophagy and apoptosis, and enhanced CXCR4 expression. si-H19 decreased p-p65 phosphorylation, while si-H19 and miR-139-3p inhibitor co-treatment partially elevated p-p65 phosphorylation. In conclusion, lncRNA H19 facilitated the autophagy and apoptosis of DNPCs by the miR-139-3p/CXCR4/NF-κB axis, thereby aggravating IDD. This study may offer new insights for the management of IDD.
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