ArticleCurrent medical science2024
FKBP5 Regulates the Osteogenesis of Human Adipose-derived Mesenchymal Stem Cells.
Article in Current medical science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Histone acetylation promotes FKBP5 to increase reparative dentin formation in pulp repair.Stem cells translational medicine · 2026Article
- Interferon-JAK-STAT Axis in Bone Metabolism.Current osteoporosis reports · 2026Review
- The mechanism and clinical significance of FKBP5 gene DNA methylation in various psychiatric, metabolic and tumor-related diseases.Frontiers in genetics · 2026Review
- FKBP5 promotes osteogenic differentiation of mesenchymal stem cells through type-I interferon pathway Inhibition.Cellular and molecular life sciences : CMLS · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveHuman 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.
methodsLentivirus 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.
resultsFollowing 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 which the osteogenesis-regulating activity of FKBP5 rests.
conclusionOur study revealed that FKBP5 enhances the osteogenesis of ASCs, providing a feasible method for clinical bone tissue engineering applications.
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