MiR-30a-5p accelerates adipogenesis by negatively regulating Sirtuin 1
Cui S., Soni CB., Xie J., Li Y., Zhu H., Wu F.
Laboratory Study, published in Int J Clin Exp Pathol (2018) — 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
- Int J Clin Exp Pathol (2018)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 31949600
- PMCID
- PMC6963029
- Citations
- 11
Abstract (original English)
Background Obesity is a chronic metabolic disease characterized by excess fat accumulation. Disordered differentiation of preadipocytes is the leading cause of adipogenesis. Thus, a clarification of the molecular mechanisms that dominate adipocyte differentiation is imperative. MiR-30a-5p is reported to involve in the modulation of multiple cellular processes, including differentiation, whereas, the role of miR-30a-5p in adipocyte differentiation is still unclear. Methods The abundances of miR-30a and Sirtuin 1 (SIRT1) mRNA were detected by RT-qPCR. SIRT1, PPARγ, C/EBPα, and FABP4 protein levels were assessed by western blot (WB). The accumulation of triglyceride (TG) was detected using Triglyceride Content Assay Kit. Cell proliferation activity was evaluated using the MTT assay. Bioinformatics software and the luciferase reporter assay were used to validate the true interaction between miR-30a-5p and SIRT1. Results miR-30a-5p expression remains increased during adipocyte differentiation of 3T3-L1 cells. The overexpression of miR-30a-5p enforced adipocyte differentiation, reflected by the enrichment of PPARγ, C/EBPα, FABP4, and triglyceride, as well as the reduction of cell proliferation. SIRT1 was identified as a target of miR-30a-5p, and a supplement of SIRT1 suppressed 3T3-L1 cell differentiation. Conclusion miR-30a-5p regulated 3T3-L1 cell differentiation by targeting STRT1
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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