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Updated: Jan 31, 2026

Preparation and In Vitro Characterization of Magnetized miR-modified Endothelial Cells
Published on: May 2, 2017
miR-144-3p Promotes Adipogenesis Through Releasing C/EBPα From Klf3 and CtBP2
Linyuan Shen1, Qiang Li2, Jinyong Wang3
1College of Animal Science and Technology, Sichuan Agricultural University, Chengdu, China.
Abstract:
MicroRNAs (miRNAs), a class of small non-coding RNAs, have been proved as novel and potent regulators of adipogenesis. A previous study has found out that miR-144-3p was a biomarker of type 2 diabetes, but the role of miR-144-3p in regulating adipogenesis was still unclear. In the present study, the expression of miR-144-3p increased in obese mice and during the 3T3-L1 differentiation process. Overexpression of miR-144-3p suppressed the expression of cell cycle regulatory factors and inhibited pre-adipocytes proliferation. Besides, overexpression of miR-144-3p accelerated lipid accumulation in adipocytes and positively regulated adipogenesis, which was also accompanied by increasing the expression of genes related to fatty acid synthesis and decreasing the expression of genes involved in fatty acid oxidation. Furthermore, luciferase activity assays indicated that miR-144-3p directly targeted Klf3 and CtBP2. The process was also confirmed by the mRNA and protein expression of Klf3 and CtBP2, which were suppressed by miR-144-3p. Furthermore, miR-144-3p targeting Klf3/CtBP2 would induce C/EBPα activity by releasing corepressors (Klf3 and CtBP2) from its promoter region. Moreover, we also observed that miR-144-3p could promote adipogenesis in mice injected with miR-144-3p agomir through tail-vein injection. Taken together, these results support that miR-144-3p can facilitate adipogenesis both in vitro and in vivo, which implies that miR-144-3p could be a target for therapeutic intervention in obesity and metabolic syndrome in the future.
Insights
MicroRNA-144-3p promotes fat cell (adipocyte) development by regulating gene expression and lipid accumulation. This microRNA (miRNA) may offer a future therapeutic target for obesity and metabolic syndrome.
Area of Science:
- Molecular Biology
- Biochemistry
- Genetics
Background:
- MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression.
- miR-144-3p is a known biomarker for type 2 diabetes, but its role in adipogenesis was unclear.
- Adipogenesis, the process of fat cell formation, is crucial in metabolic health and disease.
Purpose of the Study:
- To investigate the role of miR-144-3p in regulating adipogenesis.
- To identify the molecular targets and mechanisms through which miR-144-3p influences fat cell development.
- To assess the potential of miR-144-3p as a therapeutic target for obesity and metabolic syndrome.
Main Methods:
- Quantitative real-time PCR to measure miRNA and gene expression.
- Cell culture experiments using 3T3-L1 pre-adipocytes for overexpression studies.
- Luciferase reporter assays to confirm direct targeting of genes.
- In vivo studies involving tail-vein injection of miR-144-3p agomir in mice.
Main Results:
- miR-144-3p expression was upregulated in obese mice and during 3T3-L1 cell differentiation.
- Overexpression of miR-144-3p inhibited pre-adipocyte proliferation but promoted lipid accumulation and adipogenesis.
- miR-144-3p directly targeted and suppressed the expression of Klf3 and CtBP2, key regulators of adipogenesis.
- miR-144-3p enhanced adipogenesis in vivo, leading to increased lipid accumulation in mice.
Conclusions:
- miR-144-3p facilitates adipogenesis both in vitro and in vivo.
- The mechanism involves the suppression of Klf3 and CtBP2, leading to increased C/EBPα activity.
- miR-144-3p represents a potential therapeutic target for treating obesity and related metabolic disorders.
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