Glucocorticoids induce the differentiation of a mesenchymal progenitor cell line, ROB-C26 into adipocytes and osteoblasts, but fail to induce terminal osteoblast differentiation.
Ito S., Suzuki N., Kato S., Takahashi T., Takagi M.
Animal Study, published in Bone (2006) — 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
- Animal Study
- Journal
- Bone (2006)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 16949358
- DOI
- 10.1016/j.bone.2006.07.012
Abstract (original English)
To clarify the effects of glucocorticoids (GCs) on osteoblast and adipocyte differentiation, we investigated the effects of dexamethasone (Dex), a GC analogue on transcription factors for osteoblasts (Runx2, Dlx5 and Osterix) and adipocytes (C/EBPs such as C/EBPalpha, C/EBPbeta and C/EBPdelta, and PPARgamma2), late osteoblastic markers, bone sialoprotein (BSP) and osteocalcin (OC), and adipocyte differentiation-dependent protein, aP2 in a clonal mesenchymal progenitor cell line, ROB-C26 (C26). C26 cells were dose- and time-dependently responsive to Dex in terms of an increase in not only mRNA and protein expressions of the C/EBPs, PPARgamma2 and aP2, but also Runx2, Dlx5, BSP and OC with no induction of Osterix, which is considered to act mainly on terminal osteoblast differentiation. Cycloheximide pretreatment indicated that Dex signaling immediately increases expressions of the C/EBPs and Dlx5, while expressions of the rest of the genes require de novo protein synthesis. Continuous Dex treatment stimulated adipocyte formation, but failed to induce Osterix expression and mineralized matrix formation. However, BMP-2 treatment of Dex-treated cells induced Osterix expression and subsequent mineralized matrix formation. These results indicate that Dex up-regulates the C/EBPs followed by increasing PPARgamma2 and aP2 expressions in C26 cells to induce adipocyte differentiation, whi
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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