A novel negative regulator of adipogenesis: microRNA-363.
Chen L., Cui J., Hou J., Long J., Li C., Liu L.
Laboratory Study, published in Stem Cells (2014) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Stem Cells (2014)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 24023010
- DOI
- 10.1002/stem.1549
Abstract (original English)
The differentiation of adipose tissue-derived stromal cells (ADSCs) into adipocytes involves a highly orchestrated series of events that includes cell lineage commitment, mitotic clonal expansion, growth arrest, and terminal differentiation. However, the molecular mechanisms controlling adipogenesis are not yet completely understood. In this study, we investigated whether microRNAs (miRNAs) play a role in adipocyte differentiation. Microarray analysis was performed to determine the miRNA expression profile during ADSC differentiation, and miR-363 was found to be one of the most significantly downregulated miRNAs. We show that the overexpression of miR-363 in ADSCs inhibited mitotic clonal expansion and terminal differentiation. Furthermore, ectopic introduction of miR-363 into ADSCs markedly reduced the levels of E2F3, a key transcription factor that regulates growth and proliferation during mitotic clonal expansion. Finally, using an EGFP/RFP reporter assay, we demonstrate that miR-363 can directly target the 3'UTR of E2F3. Taken together, these results suggest that miR-363 regulates the transition from mitotic clonal expansion to terminal differentiation during adipogenesis in ADSCs, at least in part, by targeting E2F3.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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