The active form of vitamin D (1, Alpha 25-Hydroxyvitamin D3 [1α,25(OH)2D3]) has been associated with multiple cellular processes, including bone formation. 1α,25(OH)2D deficiency results in the failure of bone formation leading to significant growth retardation and severe osteopenia. The anabolic effect of 1α,25-(OH)2D3 on bone could be explained via their action on differentiated mesenchymal stem cells (MSCs) either by facilitating osteoblastogenesis or inhibiting adipogenesis. In this study, we investigated the effect of 1α,25-(OH)2D3 on osteogenic and adipogenic differentiation of hMSCs treated with 1α,25-(OH)2D3 (10-8 mol) for 21 days. Treated and untreated undifferentiated MSCs were used as controls. We examined 12,000 human genes and expressed sequences tags on the array Human Genome U95A via Affymetrix DNA array. RT PCR confirmed those genes with higher and lower expression. We found that, compared to undifferentiating MSCs, differentiating cells treated with 1α,25-(OH)2D3 exhibited a significantly higher expression (more than two-fold change significance) of distinct osteogenic genes (e.g. CYP24A1, AI131030, ITGAV, GYS1 and TBCD) and adipogenic genes ( e.g. APOE, FBLN2, SYN1, G0S2, PARRES2 and CYP24A1 ).
In addition, two genes (FBLN2 and G0S2) showed significantly high expression in adipogenic conditions while decreased in the osteogenic conditions treated with 1α,25-(OH)2D3. Meanwhile, AYP24A1, associated with 1α,25-(OH)2D3 degradation, has reduced expression in adipogenic conditions compared to osteogenic and general conditions. In summary, our gene array analyses identified a direct effect of 1α,25-(OH)2D3 on a set of genes required in MSCs differentiation, thus improving our understanding of the effect of the active form on vitamin D on bone metabolism.