基因敲除
生物
细胞生物学
脂肪组织
炎症
干细胞
NF-κB
小RNA
促炎细胞因子
癌症研究
NFKB1型
肿瘤坏死因子α
免疫学
转录因子
细胞培养
内分泌学
基因
遗传学
作者
Chanyuan Jin,Lingfei Jia,Yiping Huang,Yunfei Zheng,Ning Du,Yunsong Liu,Yongsheng Zhou
出处
期刊:Stem Cells
[Oxford University Press]
日期:2016-06-23
卷期号:34 (11): 2707-2720
被引量:100
摘要
Abstract Osteogenic differentiation and bone formation is suppressed under condition of inflammation induced by proinflammation cytokines. A number of studies indicate miRNAs play a significant role in tumor necrosis factor-α-induced inhibition of bone formation, but whether long non-coding RNAs are also involved in this process remains unknown. In this study, we evaluated the role of MIR31HG in osteogenesis of human adipose-derived stem cells (hASCs) in vitro and in vivo. The results suggested that knockdown of MIR31HG not only significantly promoted osteogenic differentiation, but also dramatically overcame the inflammation-induced inhibition of osteogenesis in hASCs. Mechanistically, we found MIR31HG regulated bone formation and inflammation via interacting with NF-κB. The p65 subunit bound to the MIR31HG promoter and promoted MIR31HG expression. In turn, MIR31HG directly interacted with IκBα and participated in NF-κB activation, which builds a regulatory circuitry with NF-κB. Targeting this MIR31HG–NF-κB regulatory loop may be helpful to improve the osteogenic capacity of hASCs under inflammatory microenvironment in bone tissue engineering.
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