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MicroRNA-142 protects MC3T3-E1 cells against high glucose-induced apoptosis by targeting β-catenin
Tiansheng Zheng1, Guanglin Ji1, Jincai Chen1
1Department of Orthopedics, The First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi 341000, P.R. China.
Abstract:
Osteoporosis, characterized by decreased mineral density and bone mass, is triggered by various detrimental factors and often causes further complications, including fractures. Aberrant expression of microRNAs (miRs) has been associated with the pathogenesis of osteoporosis. Recently, miR-142 was reported to be downregulated in osteoblasts; however, the underlying mechanism of miR-142 in mediating the development of osteoporosis remains unclear. In the present study, high glucose induced the downregulation of miR-142 mRNA expression and promoted the apoptosis of MC3T3-E1 cells. miR-142-mimics significantly protected against high glucose-induced apoptosis, upregulated the expression levels of B-cell lymphoma 2 (Bcl-2) and downregulated the protein expression levels of β-catenin, Bcl-2 associated X (Bax) and caspase-3. Furthermore, β-catenin was identified as a direct target of miR-142 using luciferase reporter assays. Similar to the effects of miR-142 inhibitors, overexpression of β-catenin aggravated the apoptosis of MC3T3-E1 cells, as demonstrated by the upregulation of Bax and caspase-3, and the downregulation of Bcl-2 expression levels. In conclusion, miR-142 protects MC3T3-E1 cells against high glucose-induced apoptosis by targeting β-catenin.
Insights
MicroRNA-142 (miR-142) protects bone cells from high glucose-induced apoptosis. This study reveals miR-142 targets beta-catenin, offering a new therapeutic target for osteoporosis.
Area of Science:
- Biochemistry
- Molecular Biology
- Cell Biology
Background:
- Osteoporosis involves decreased bone density and mass, leading to fractures.
- Aberrant microRNA (miRNA) expression is implicated in osteoporosis pathogenesis.
- The role of miR-142 in osteoporosis development is not fully understood.
Purpose of the Study:
- To investigate the mechanism of miR-142 in high glucose-induced osteoblast apoptosis.
- To determine if miR-142 can protect against high glucose-induced apoptosis in MC3T3-E1 cells.
- To identify the direct target of miR-142 involved in this process.
Main Methods:
- MC3T3-E1 cells were treated with high glucose.
- miR-142 mimics and inhibitors were used to modulate miR-142 levels.
- Apoptosis, Bcl-2, Bax, caspase-3, and beta-catenin expression were assessed.
- Luciferase reporter assays identified beta-catenin as a direct miR-142 target.
Main Results:
- High glucose downregulated miR-142 and induced MC3T3-E1 cell apoptosis.
- miR-142 mimics reduced apoptosis and modulated apoptosis-related proteins (Bcl-2, Bax, caspase-3).
- Beta-catenin was confirmed as a direct target of miR-142; its overexpression mimicked miR-142 inhibition effects.
Conclusions:
- miR-142 protects osteoblasts against high glucose-induced apoptosis.
- This protective effect is mediated by targeting beta-catenin.
- miR-142 represents a potential therapeutic target for managing high glucose-related bone loss.
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