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Updated: Feb 17, 2026
An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function
Published on: May 4, 2021
Study of microRNAs targeted Dvl2 on the osteoblasts differentiation of rat BMSCs in hyperlipidemia environment
Xin Huang1, Zhifeng Wang2, Duoduo Li1
1Department of Prosthodontics, School of Dentistry, Shandong University, Jinan, China.
Abstract:
Dishevelled 2 (Dvl-2), a key mediator of the wnt/β-catenin signaling pathway, plays critical roles in osteoblasts differentiation in hyperlipidemia environment. In our previous study, we observed a strong correlation between increased dvl2 expression and decreased new bone formation around implants in a rat hyperlipidemia implant surgery model. However, transcriptional regulation of Dvl2 by microRNAs in this process remains unknown. In the current study, we searched in online database and identified four significantly up-regulated miRNAs, miR-21-5p, miR-29c-3p, miR-138-5p, and miR-351-5p that could potentially regulate Dvl2. Using Western blot and dual-luciferase assays, we confirmed that miR29c-3p suppresses Dvl2 expression by binding to its 3'-UTR. Our results suggest a novel transcriptional regulation mechanism of Dvl2 by miR-29c-3p in osteoblasts differentiation of BMSCs.
Insights
MicroRNAs regulate Dishevelled 2 (Dvl-2) in bone cells. Specifically, miR-29c-3p suppresses Dvl-2, impacting osteoblast differentiation in hyperlipidemia, revealing a new regulatory mechanism for bone formation.
Area of Science:
- Biochemistry
- Molecular Biology
- Regenerative Medicine
Background:
- Dishevelled 2 (Dvl-2) is crucial for wnt/β-catenin signaling and osteoblast differentiation, particularly in hyperlipidemic conditions.
- Previous research linked increased Dvl-2 expression to reduced bone formation in hyperlipidemia models.
- The microRNA-mediated transcriptional regulation of Dvl-2 in this context was previously unknown.
Purpose of the Study:
- To investigate the role of microRNAs in regulating Dishevelled 2 (Dvl-2) expression during osteoblast differentiation.
- To identify specific microRNAs that target and modulate Dvl-2 in a hyperlipidemia environment.
- To elucidate the precise mechanism by which microRNAs control Dvl-2 in bone cells.
Main Methods:
- Bioinformatic analysis to identify potential microRNA targets of Dvl-2.
- Western blot analysis to assess Dvl-2 protein levels.
- Dual-luciferase reporter assays to confirm direct binding of microRNAs to the Dvl-2 3'-UTR.
Main Results:
- Four microRNAs (miR-21-5p, miR-29c-3p, miR-138-5p, miR-351-5p) were identified as potential regulators of Dvl-2.
- miR-29c-3p was confirmed to directly bind to the 3'-untranslated region (3'-UTR) of Dvl-2.
- miR-29c-3p was shown to suppress Dvl-2 expression at the transcriptional level.
Conclusions:
- A novel regulatory pathway involving miR-29c-3p suppressing Dvl-2 expression in osteoblasts was discovered.
- This finding provides new insights into the molecular mechanisms governing osteoblast differentiation in hyperlipidemia.
- The miR-29c-3p/Dvl-2 interaction represents a potential therapeutic target for modulating bone formation in related conditions.
