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OLMALINC alleviates dexamethasone-induced osteoporosis via targeting miR-124-3p
Siyuan Ha1, Jing Xiao2, Ning Gan3
1Anesthesiology, The Wuhan Hospital of TCM Affiliated to Hubei University of Traditional Chinese Medicine, Wuhan, China.
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.
Insights
Long non-coding RNA OLMALINC plays a crucial role in mitigating dexamethasone-induced osteoporosis by regulating osteoblast function. OLMALINC counteracts the negative effects of dexamethasone on bone cells, highlighting its therapeutic potential.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- Osteoporosis is a significant health concern, often exacerbated by treatments like dexamethasone.
- Dexamethasone impairs osteoblast differentiation, leading to reduced bone formation and increased fracture risk.
- Understanding the molecular mechanisms underlying dexamethasone-induced osteoblast dysfunction is critical for developing effective therapies.
Purpose of the Study:
- To elucidate the role of long non-coding RNA (lncRNA) OLMALINC in dexamethasone (Dex)-induced impairment of osteoblast differentiation and osteoporosis.
- To investigate the regulatory relationship between OLMALINC and microRNA-124-3p (miR-124-3p) in the context of Dex treatment.
Main Methods:
- MC3T3-E1 cells were used for gain and loss-of-function experiments to assess OLMALINC and miR-124-3p impacts.
- Dual-luciferase reporter assays, RNA pull-down, and MS-RIP confirmed the interaction between OLMALINC and miR-124-3p.
- RT-qPCR, Western blot, flow cytometry, and CCK-8 assays quantified gene/protein expression, apoptosis, and cell viability.
Main Results:
- Dexamethasone treatment decreased OLMALINC expression while increasing miR-124-3p levels.
- Overexpression of OLMALINC counteracted Dex-induced osteogenic damage, enhancing cell viability and osteogenic markers (OPG, ALP, Runx2).
- OLMALINC directly targets and negatively regulates miR-124-3p; conversely, miR-124-3p mimic reversed OLMALINC's protective effects.
Conclusions:
- The OLMALINC/miR-124-3p axis is a key regulator in dexamethasone-induced osteoblast differentiation impairment and osteoporosis.
- This axis influences osteoblast function by modulating cell viability, apoptosis, and the expression of critical osteogenic factors.