ArticleStem cell research & therapy2026
Dexamethasone reduces osteogenic potential through suppressing retinoic acid signaling via NF-κB/CYP26B1 axis in mesenchymal stem cells.
Article in Stem cell research & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveGlucocorticoid-induced osteoporosis (GIOP) is the most common secondary osteoporosis, which characterized by the decreased bone strength and increased fracture risk. But the pathogenic causes of GIOP remains not completely yet. In this study, we investigated the effect of Cyp26b1, a key enzyme for all-trans retinoic acid (ATRA) degradation, on the osteogenic inhibitory effect of dexamethasone (DEX) in mesenchymal stem cells (MSCs) and revealed the possible mechanism through which DEX regulates the expression of Cyp26b1.
methodsMSCs were induced with osteogenic induction medium in vitro to establish the osteogenic model, and high concentration (10
resultsDEX (10
conclusionThe osteogenic inhibitory effect of high concentration of DEX may be resulted from the disturbance of retinoic acid signaling. The expression of Cyp26b1 can be up-regulated by either low or high concentration of DEX, but its degradation can only be inhibited by high concentration of DEX. The effect of DEX on Cyp26b1 expression was partially mediated by activating NF-κB signaling in MSCs.
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