Effects Of TUG1 On Dexamethasone-induced Apoptosis In Mouse MC3T3-E1 Cells

Objective: Osteoporosis is a common metabolic disease,and glucocorticoid osteoporosis is the most common type of secondary osteoporosis.Clinically,glucocorticoids(GC)are commonly used in the treatment of autoimmune diseases.Studies have shown that the use of glucocorticoids is likely to lead to bone density reduction and bone microstructural changes,and even osteoporosis in severe cases,we call it Glucocorticoid-induced osteoporosis(GIOP).Osteoblasts are the key factors for bone formation.Therefore,factors affecting the growth and apoptosis of osteoblasts can affect bone density,bone microstructure,and bone fragility.Long non-coding RNA(LncRNA)TUG1 is involved in the apoptosis process of osteosarcoma cells.Since osteoblasts are precursor cells of osteosarcoma cells,we hypothesized that TUG1 may be involved in the apoptosis of osteoblasts.This study was designed to investigate the effect of TUG1 on dexamethasone-induced apoptosis in mouse osteoblast MC3T3-E1 cells and its possible mechanism.Methods: Mouse osteoblast MC3T3-E1 was cultured in vitro.Apoptosis was induced by dexamethasone and serum-free starvation.Total RNA was extracted and real-time quantitative PCR(qPCR)was used to detect TUG1 in mouse MC3T3-E1.The relative expression of cells demonstrated that dexamethasone can inhibit the expression of TUG1 in cells.The experiments were divided into four groups: control group,dexamethasone group,TUG1 overexpression plasmid + dexamethasone group,negative plasmid group + dexamethasone group.Apoptosis of MC3T3-E1 cells was induced by 10 ?M dexamethasone.The cells were transfected with TUG1 overexpression plasmid and control plasmid.Apoptosis was detected by flow cytometry and ELISA.The expression of Bcl-2 was detected by immunofluorescence.Results:(1)MC3T3-E1 cells can express TUG1;(2)Dexamethasone can induce osteoblast apoptosis;(3)Overexpression of TUG1 significantly inhibited dexamethasone-induced apoptosis in MC3T3-E1 cells;(4)Overexpression of TUG1 up-regulates the expression of Bcl-2?Conclusion: TUG1 may inhibit the apoptosis of mouse MC3T3-E1 cells induced by dexamethasone by up-regulating the expression of Bcl-2,which may be a protective factor for glucocorticoid-induced osteoblast apoptosis.