In our study for that reason was to measure the ramifications of temporary hypoxia on hMSC osteogenic potential by drawing up transcriptional profiles of osteoblast membranous and order Bazedoxifene extra cellular matrix molecules, those of a factor stimulating osteoblast differentiation and those of a factor regulating bone formation. Our results show a slight down regulation of cbfa 1/ Runx2 expression occurs after temporary exposure to hypoxia, persisting for 14 days after the end of the hypoxic episode. Cbfa 1/Runx2 transcription factor plays a vital part in controlling osteoblastic differentiation and its inhibition is related to a big decrease in the rate of bone formation. Similar long-lasting inhibition of osteocalcin, a late osteogenic differentiation sign, confirmed the inhibition of osteoblastic growth of hMSCs resulting from temporary exposure to hypoxia. As occurred with type I collagen, its degree of expression was durably and strongly inhibited by temporary experience of hypoxia. Type I collagen could be the main element of bone matrix and plays a key position in the mineralization process. Longterm inhibition of cbfa 1/ Runx2, Lymph node osteocalcin and type I collagen expressions strongly suggest that temporary contact with hypoxia may possibly inhibit the osteoblastic differentiation of hMSCs. Literature performed on other cell types studies that their osteogenic differentiation is reduced by temporary experience of hypoxia. Alternatively, Salim et al. reported that exposure of hMSCs to hypoxic conditions did not affect their terminal differentiation. The discrepancies observed between that study and our results may be reversible Chk inhibitor described by different time of exposure to hypoxic conditions, suggesting that hMSCs can face hypoxia for a short period of time without loosing their osteogenic potential. Remarkably, neither the expression of BSP, which is regulated by cbfa 1/Runx2 at both mRNA and protein levels, or that of ALP, the enzymatic action of which has been previously reported to be down regulated under hypoxic conditions, were found here to be affected by temporary exposure to hypoxia. In the event of BSP expression, the down regulation of cbfa 1/Runx2 seen in the present study might be too weak to notably inhibit BSP expression. Moreover, Park et al. have reported that the inhibitory effect of hypoxia on the osteoblastic differentiation of a osteosarcoma cell line is time dependent: the longer the hypoxic exposure time, the greater the down regulation of osteoblastic marker expression. These results declare that exposure times longer than those used in the current study may possibly nevertheless produce a regulation of mRNA expression of BSP or ALP. Osteopontin phrase by hMSCs was permanently improved, on the other hand, by temporary exposure to hypoxia.