miR-33a hinders the differentiation of adipose mesenchymal stem cells towards urothelial cells in an inductive condition by targeting β‑catenin and TGFR.
Fan G., Xu Z., Hu X., Li M., Zhou J., Zeng Y.
Laboratory Study on Scar, published in Mol Med Rep (2017) — 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
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- Study type
- Laboratory Study
- Journal
- Mol Med Rep (2017)
- Country
- Greece
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 29207162
- PMCID
- PMC5783476
- DOI
- 10.3892/mmr.2017.8168
- Citations
- 5
Abstract (original English)
Tissue engineering technology offers an appealing approach for tissue reconstruction of the urothelium. Adipose‑derived mesenchymal stem cells (ADSCs) represent an abundant source for tissue engineering applications. However, ASCs primarily possess mesoderm lineage differentiation potential. It is difficult to induce differentiation of ASCs towards urothelial cells that are derived from the endoderm, although a recent findings have reported that a conditioned medium may drive ADSCs towards differentiation into the urothelium phenotype. In the present study, human ADSCs were isolated from abdominal adipose tissues and incubated in this conditioned medium for indicated time periods. Western blotting showed that protein expression levels of urothelial specific marks, including CK7, CK20 and UPIII, were increased after seven days' incubation, but immunofluorescence microscopy determined that cells with CK7 and UPIII staining were scarce, which suggested a low‑efficiency for the differentiation. Prolonging the incubation time did not further increase CK20 and UPIII expression. Furthermore, miR‑33a expression was increased with ADSC differentiation. Using synthetic miRNAs to mimic or inhibit the action of miR‑33a revealed that miR‑33a hinders the differentiation of ADSCs towards urothelial cells. Furthermore, luciferase reporter assay confirmed that β‑catenin and transforming growth
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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