FKBP5 Regulates the Osteogenesis of Human Adipose-derived Mesenchymal Stem Cells.
Tian XY., Zhu B., Fang WC., Zhou XB., Wu N., Li H.
Laboratory Study, published in Curr Med Sci (2024) — 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
- Curr Med Sci (2024)
- Country
- China
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 39586968
- DOI
- 10.1007/s11596-024-2941-8
- Citations
- 2
Abstract (original English)
Objective Human adipose-derived stem cells (ASCs) have shown considerable potential for tissue regeneration. FK506 binding protein (FKBP) 5 is a cochaperone of several proteins. The purpose of this work was to explore the function of FKBP5 in ASC osteogenesis. Methods Lentivirus infection was used to overexpress or knock down FKBP5 in ASCs. To inhibit FKBP5, SAFit2, a specific inhibitor of FKBP5, was used. Next, the osteogenic capacity of ASCs was evaluated via alkaline phosphatase (ALP) staining, and extracellular calcium precipitation was detected via Alizarin red S staining. The binding proteins of FKBP5 were assessed via proteomics and validated via coimmunoprecipitation experiments. Results Following osteogenic induction, FKBP5 expression increased at both the mRNA and protein levels. Interestingly, FKBP5 upregulation by lentivirus infection increased the ability of ASCs to differentiate into osteoblasts, as revealed by ALP staining, while ALP activity also increased. Moreover, increased extracellular calcium precipitation confirmed that FKBP5 overexpression promoted ASC osteogenesis into osteocytes. On the other hand, FKBP5 knockdown or functional suppression with SAFit2 decreased this process. Furthermore, the proteomics and coimmunoprecipitation data demonstrated that FKBP5 bound to a variety of proteins in ASCs. These proteins serve as the molecular chaperone base upon
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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