A combination of insulin and ubiquitin A20 promotes osteocalcin expression in adipose-derived stem cells.
Wang L., Xu X., Huo N., Guo H., Wang D., Liu H.
Laboratory Study, published in Biochem Cell Biol (2013) — 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
- Biochem Cell Biol (2013)
- Country
- Canada
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 24219294
- DOI
- 10.1139/bcb-2013-0043
- Citations
- 2
Abstract (original English)
Osteocyte generation can be used in bone defect repair; the generation efficiency needs to be further improved. This study aims to evaluate the role of ubiquitin A20 (A20) in facilitating the expression of osteocalcin in adipose-derived stem cells (ADSCs). In this study, adipose tissue was obtained from 10 healthy human subjects; ADSCs were isolated from the adipose samples. The ADSCs were transfected with core binding factor alpha 1 (Cbfa1) and/or insulin-like growth factor-1 receptor (IGF-1R). Expression of osteocalcin, A20 in ADSCs was assessed by quantitative RT-PCR (qRT-PCR) and Western blotting. Apoptosis of ADSCs was analyzed by flow cytometry. The results showed that after the gene transfection and stimulation of insulin, the ADSCs expressed high levels of osteocalcin. However, apoptotic ADSCs were induced by the activation of IGF-1R. Exposure to insulin down-regulated the expression of Bcl-xL and A20, and increased Bax, in ADSCs. The addition of exogenous A20 prevented the ADSC apoptosis. We conclude that activation of IGF-1R can induce apoptosis in ADSCs, which can be prevented by addition of exogenous A20.
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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