Transforming growth factor β1 (TGF-β1) has been suggested to be a candidate cytokine in the field of bone tissue engineering. Cytokines serve important roles in tissue engineering, particularly in the repair of bone damage; however, the underlying molecular mechanisms remain unclear. In the present study, the effects of TGF-β1 on the osteogenesis and motility of hFOB1.19 human osteoblasts were demonstrated via the phenotype and gene expression of cells. Additionally, the role of the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin/S6 kinase 1 (PI3K/AKT/mTOR/S6K1) signalling pathway in the effects of TGF-β1 on osteoblasts was investigated. It was demonstrated using Cell Counting Kit-8 and flow cytometry assays that the proliferation of human osteoblasts was promoted by 1 ng/ml TGF-β1. In addition, alkaline phosphatase activity, Alizarin red staining, scratch-wound and Transwell assays were conducted. It was revealed that osteogenesis and the migration of cells were regulated by TGF-β1 via the upregulation of osteogenic and migration-associated genes. Alterations in the expression of osteogenesis- and migration-associated genes were evaluated following pre-treatment with a PI3K/AKT inhibitor (LY294002) and an mTOR/S6K1 inhibitor (rapamycin), with or without TGF-β1. The results indicated that TGF-β1 affected the osteogenesis and mineralisation of osteoblasts via the PI3K/AKT signalling pathway. Furthermore, TGF-β1 exhibited effects on mTOR/S6K1 downstream of PI3K/AKT. The present study demonstrated that TGF-β1 promoted the proliferation, differentiation and migration of human hFOB1.19 osteoblasts, and revealed that TGF-β1 affected the biological activity of osteoblasts via the PI3K/AKT/mTOR/S6K1 signalling pathway. Our findings may provide novel insight to aid the development of bone tissue engineering methods for the treatment of bone injury.
Hexagonal BaAl 2 O 4 :Eu 2þ , Dy 3þ polynary complex nanotubes with long-lasting phosphorescence were obtained through a facile coprecipitation approach followed by a postcalcining reaction in a weak reducing atmosphere. In the case of low annealing temperature, anion vacancies and surface stress can induce lattice contraction due to poor crystallininty; moreover, Eu 2þ ions can occupy two different crystallographic Ba 2þ sites due to low symmetry, resulting in an appearance of double emission peaks. For the sample annealed at higher temperature, however, Eu 2þ ions only occupy substitutedly the Ba 2þ sites with lowest energy due to high crystallinity; moreover, as compared to the sample annealed at low temperature, its emission band redshifts as the results of both high crystal symmetry around Eu 2þ ions and large average optical path. Additionally, Eu 2þ and Dy 3þ ions substitute incompletely for Ba 2þ sites in nanostructures, leading to the decrease of effective electron trap densities and depths, and therefore tubular nanostructures show fast afterglow decay rate in comparison with the bulk counterpart.
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