OLMALINC alleviates dexamethasone-induced osteoporosis via targeting miR-124-3p.

Abstract

Introduction and objective: This study aims to investigate the mechanism of LncRNA(lncRNAs) OLMALINC in dexamethasone (Dex)-induced osteoblast differentiation impairment and osteoporosis.

Material and methods: To investigate the impact of OLMALINC and miR-124-3p on Dex-treated osteoblasts, functional gain and loss experiments were conducted using MC3T3-E1 cells. Dual-luciferase reporter assays, RNA pull-down, and MS-RIP experiments were used to verify the targeting relationship between OLMALINC and miR-124-3p. RT-qPCR was conducted to analyze OLMALINC and miR-124-3p levels, as well as osteogenic regulatory factors OPG, Runx2, and ALP-related mRNA in different treatment groups. Protein expression levels were determined by Western blot analysis. Apoptosis was assessed by flow cytometry. cell viability was assessed by CCK-8.

Results: After Dex treatment, OLMALINC levels decreased, while miR-124-3p increased. Transfection of oe-OLMALINC counteracted Dex-induced osteogenic damage by increasing cell viability, decreasing apoptosis reduction, stimulating OPG, ALP, and Runx2 stimulation. OLMALINC targeted miR-124-3p, with OLMALINC negatively regulating miR-124-3p. In turn, miR-124-3p mimic reversed the protective effect of OLMALINC against Dex-induced osteoblast dysfunction.

Conclusions: These results indicate that the OLMALINC/miR-124-3p axis influences osteoblast differentiation in Dex-induced osteoblast differentiation impairment and osteoporosis by regulating cell viability, apoptosis, and osteogenic factors.