Effects of LncRNA SNHG15 on Osteogenic/Adipogenic Differentiation of Bone Marrow Mesenchymal Stem Cells Under Oxidative Stress by TGFβ/Smad Signaling Pathway

Abstract

Oxidative stress can affect bone marrow mesenchymal stem cells (BMSCs). LncRNA SNHG15 involves in a variety of cellular physiological and pathological processes. However, LncRNA SNHG15’s effect on osteogenesis/adipogenic differentiation of BMSCs under oxidative stress remains unclear. BMSCs were divided into normal control group; oxidative stress group; SNHG15 group in which SNHG15 plasmid was transfected under oxidative stress condition followed by analysis of the expression of LncRNA SNHG15, RUNX2 and OPN by real-time quantitative PCR, reactive oxygen species (ROS) and superoxide dismutase (SOD) activity, FABP4 and PPARγ2 mRNA expression, alkaline phosphatase (ALP) activity and TGFβ/Smad signaling by Western blot. Under oxidative stress, the expression of SHHG15, RUNX2 and OPN mRNA was significantly decreased, ROS production was increased, SOD activity was reduced, along with increased expression of FABP4 and PPARγ2 protein, decreased ALP activity, as well as reduced expression of TGFβ1, Smad2, and Smad7 compared to control group (P < 0.05). Transfection of LncRNA SNHG15 plasmid significantly up-regulated the expression of SNHG15, RUNX2 and OPN mRNA, decreased ROS production, increased SOD activity, decreased expression of FABP4 and PPARγ2 mRNA, and increased ALP activity as well as increased expression of TGFβ1, Smad2, and Smad7 compared to control group (P < 0.05). The expression of SNHG15 is decreased in BMSCs under oxidative stress. Up-regulation of SNHG15 expression can improve the redox balance through TGFβ/Smad signaling pathway, promote osteogenic differentiation of BMSCs under oxidative stress, and inhibit its differentiation into fat.