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Dexamethasone (Dex) caused impaired osteoblast differentiation and oxidative stress (OS) in bone marrow mesenchymal stem cells (BMSCs). This work sought to elucidate the precise molecular pathway through which Dex influences osteogenic differentiation (OD) and OS in BMSCs.Methods    The expression of Runt-related transcription factor 1 (RUNX1) and alpha-2 macroglobulin (A2M) was assessed in Dex-treated BMSCs using qRT-PCR and Western Blot. Following the functional rescue experiments, cell proliferation was determined by MTT assay, reactive oxygen species (ROS) expression by DCFH-DA fluorescent probe, lactate dehydrogenase (LDH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (Gpx) expression by kits, OD by alkaline phosphatase (ALP) staining and activity quantification, and the expression of OD-related proteins RUNX2, collagen type 1 alpha 1 (COL1A1), and osteocalcin (OCN) by qRT-PCR and Western Blot. The binding of RUNX1 to A2M was initially analyzed through Jaspar website and subsequently verified by dual-luciferase reporter and ChIP assays.Results    Dex-treated BMSCs had low RUNX1 and A2M expression. Dex treatment apparently elevated ROS and LDH levels, diminished cell proliferation rate and SOD, CAT, and Gpx expression, lightened intensity of ALP staining, and declined calcified nodules, ALP activity, and RUNX2, COL1A1, and OCN expression in BMSCs, which was counterweighed by RUNX1 or A2M overexpression. RUNX1 positively targeted A2M. A2M knockdown effectively nullified the ameliorative effects of RUNX1 overexpression on impaired OD and OS injury in Dex-induced BMSCs.Conclusions    Overexpression of RUNX1 attenuated Dex-induced impaired OD and OS injury in BMSCs by promoting A2M transcription.

biocell

Overexpression of RUNX1 mitigates dexamethasone-induced impairment of osteogenic differentiation and oxidative stress injury in bone marrow mesenchymal stem cells by promoting alpha-2 macroglobulin transcription