Open AccessInhibition of lncRNA MIR31HG Promotes Osteogenic Differentiation of Human Adipose‐Derived Stem Cells
Author(s) -
Jin Chanyuan,
Jia Lingfei,
Huang Yiping,
Zheng Yunfei,
Du Ning,
Liu Yunsong,
Zhou Yongsheng
Publication year - 2016
Publication title -
stem cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.159
H-Index - 229
eISSN - 1549-4918
pISSN - 1066-5099
DOI - 10.1002/stem.2439
Subject(s) - gene knockdown , microbiology and biotechnology , biology , stem cell , adipose tissue , inflammation , proinflammatory cytokine , nf κb , mesenchymal stem cell , microrna , cancer research , cellular differentiation , immunology , cell culture , endocrinology , gene , genetics
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. S tem C ells 2016;34:2707–2720