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Methylation of miR-145a-5p promoter mediates adipocytes differentiation
Jingjing Du1, Xiao Cheng1, Linyuan Shen1
1College of Animal Science and Technology, Sichuan Agricultural University, Chengdu 611130, China.
Abstract:
MicroRNAs (miRNAs, miR) play important roles in adipocyte development. Recent studies showed that the expression of several miRNAs is closely related with promoter methylation. However, it is not known whether miRNA mediates adipocytes differentiation by means of DNA methylation. Here, we showed that miR-145a-5p was poorly expressed in adipose tissue from mice fed a high fat diet (HFD). Overexpression or inhibition of miR-145a-5p was unfavorable or beneficial, respectively, for adipogenesis, and these effects were achieved by regulating adipocyte-specific genes involved in lipogenic transcription, fatty acid synthesis, and fatty acid transportation. Particularly, we first suggested that miR-145a-5p mimics or inhibitors promoted or repressed adipocytes proliferation by regulating p53 and p21, which act as cell cycle regulating factors. Surprisingly, the miR-145a-5p-repressed adipocyte differentiation was enhanced or rescued when cells treated with 5-Aza-dC were transfected with miR-145a-5p mimics or inhibitors, respectively. These data indicated that, as a new mean to positively regulate adipocyte proliferation, the process of miR-145a-5p-inhibited adipogenesis may be regulated by DNA methylation.
Insights
MicroRNA-145a-5p negatively impacts adipogenesis by regulating key genes and cell cycle factors. Its effects on adipocyte differentiation appear to be mediated by DNA methylation, offering a new regulatory mechanism.
Area of Science:
- Molecular Biology
- Genetics
- Cell Biology
Background:
- MicroRNAs (miRNAs) are crucial regulators of adipocyte development.
- miRNA expression is often linked to DNA methylation, but the role of miRNAs in mediating DNA methylation during adipogenesis is unclear.
Purpose of the Study:
- To investigate the role of miR-145a-5p in adipocyte differentiation and proliferation.
- To determine if miR-145a-5p mediates adipogenesis through DNA methylation.
Main Methods:
- Analysis of miR-145a-5p expression in mice fed a high-fat diet.
- Overexpression and inhibition of miR-145a-5p in adipocytes.
- Assessment of adipocyte-specific gene expression.
- Investigation of cell cycle regulators p53 and p21.
- Treatment with 5-Aza-dC (a DNA methylation inhibitor) in conjunction with miR-145a-5p manipulation.
Main Results:
- miR-145a-5p expression was reduced in adipose tissue from high-fat diet-fed mice.
- miR-145a-5p overexpression impaired adipogenesis, while inhibition was beneficial.
- miR-145a-5p regulated genes involved in lipogenesis and fatty acid metabolism.
- miR-145a-5p influenced adipocyte proliferation by targeting p53 and p21.
- DNA methylation inhibition (5-Aza-dC) modulated the effects of miR-145a-5p on adipocyte differentiation, suggesting a regulatory link.
Conclusions:
- miR-145a-5p plays a significant role in regulating adipogenesis and adipocyte proliferation.
- The inhibitory effect of miR-145a-5p on adipogenesis may be regulated by DNA methylation.
- This study identifies a novel mechanism linking miRNA, DNA methylation, and adipogenesis.
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