You are hereNovember 21, 2016 | Adipose Stem Cells
LncRNA Loss gives hASCs a Bone Boost!
Review of “Inhibition of lncRNA MIR31HG Promotes Osteogenic Differentiation of Human Adipose-Derived Stem Cells” from Stem Cells by Stuart P. Atkinson
Mesenchymal stem cells derived from our all-too-plentiful (!) adipose tissue (human adipose stem cells or hASCs) hold great potential for the repair of bone defects. One of the barriers to successful bone repair is the inflammatory environment which greets transplanted hASCs at site of injury . Unfortunately, this stress-filled environment inhibits osteogenic differentiation of hASCs and subsequent bone formation .
Multiple strategies to improve hASC osteogenesis have been proposed, but a new study from the lab of Yongsheng Zhou (Peking University, Beijing, China) may have now uncovered a novel and effective method. In their new Stem Cells study, Jin et al report that the knockdown of the long non-coding RNA (lncRNA) MIR31HG [3, 4] efficiently boosts the osteogenic capabilities of hASCs in an inflamed microenvironment .
But why look at MIR31HG? The authors understood both that the presence of inflammatory cytokines (e.g. TNF-α and IL-17) inhibited hASC osteogenesis via the potentiation of NF-κB signaling and that the MIR31HG promoter contained NF-κB binding sites . Subsequent in vitro analysis of hASCs confirmed that inflammatory signaling boosted MIR31HG expression via the direct binding of NF-κB to the MIR31HG promoter and that the elevated levels of MIR31HG correlated to a decrease in hASC osteogenesis. MIR31HG achieved this decrease by interacting with an NF-κB inhibitor (IκBα) thereby promoting the osteogenic inhibitory activity of NF-κB itself. However, the authors also found that the shRNA-mediated knockdown of MIR31HG under inflammatory conditions in vitro and in vivo permitted an increase in hASC osteogenic potential and permitted the formation of bone.
The identification of an MIR31HG–NF-κB regulatory loop both confirms the importance of lncRNAs to the osteogenic differentiation of hASCs and provides us with new targets for improved bone-related regenerative therapies under inflammatory conditions. It seems that lncRNA loss is sufficient to give ASCs a bone boost; what other RNA species play roles?
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