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ABSTRACT
Purpose: Mesenchymal stem cells (MSCs) are a reliable cell source for tissue regeneration. However, the molecular mechanisms underlying the directed differentiation of MSCs remain unclear which impedes potential clinical applications. Recent studies have discovered that Homeobox (HOX) genes are involved in the differentiation regulation of MSCs and bone formation. In this study, we investigate the HOXC10 function in the osteogenic differentiation potential of MSCs. Materials and Methods: Stem cells from apical papilla (SCAPs) and adipose-derived stem cells (ADSCs) were used in this study. Alkaline phosphatase (ALP) activity assays, ALP staining, Alizarin red staining, quantitative calcium analysis, osteogenesis-associated gene expression, and in vivo transplantation experiments were used to study osteogenic differentiation potential. Results: Our results showed that overexpression of HOXC10 in SCAPs inhibited ALP activity and mineralization in vitro and decreased the mRNA expression of collagen alpha-1 (I) chain, bone sialoprotein, osteocalcin, and a key transcription factor, runt-related transcription factor 2, in SCAPs. Depletion of HOXC10 promoted osteogenic differentiation in SCAPs in vitro. In addition, in vivo transplantation experiments in nude mice confirmed that SCAPs osteogenesis was triggered when HOXC10 was downregulated. Furthermore, depletion of HOXC10 also enhanced osteogenic differentiation in ADSCs. Conclusions: Taken together, these results indicated that HOXC10 decreased the MSC osteogenic differentiation potential. Thus, inhibition of HOXC10 in MSCs might have the potential to improve tissue regeneration and provide insight into the mechanism underlying the directed differentiation of MSCs.
Declaration of interest
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the article.
Funding
This work was supported by grants from the National Natural Science Foundation of China (81625005 to Z.P.F.), Beijing Natural Science Foundation (7172089 to Z.P.F.), and Beijing Scholar Program (PXM2016_014226_000034, PXM2016_014226_000006, PXM2015_014226_000116, PXM2015_014226_000055, PXM2015_014226_000052).
Supplemental Material
Supplemental data for this article can be accessed on the publisher’s website.
