中文摘要：

我们的以前的研究证明了砷三氧化物(ATO ) 在与无形的贫血症(AA ) 对待病人有临床的功效。然而，机制尚待被阐明。骨头髓的重要部件造血的微型环境，骨头髓间充质的干细胞(BMSC ) ，经常在 AA 病人被改变。在这研究， AA BMSC 是容易的被导致进 adipocytes 而非造骨细胞，这被发现。ATO 治疗能部分至少恢复 AA BMSC 的区别不平衡。我们进一步在 AA BMSC 区别作为一个关键管理者识别了 miR-204。酶记者试金证明 miR-204 能直接绑在 Runx2 mRNA 的 3-untranslated 区域，调整成骨的一个关键抄写因素。而且， adipogenic 区别被支持， osteogenic 区别在 miR-204 被禁止过去表示的房间而成骨被提高， adipocyte 形成在房间被禁止，那失去了 miR-204 功能，它建议了它的内长的功能。一起我们证明 ATO 能禁止 adipogenic 区别，但是在 AA BMSC 支持 osteogenic 区别，在 AA 病人为 ATO 临床的功效提供可能的解释。MiR-204 戏在调整 BMSC 区别的一个关键角色，和下面调整的 miR-204 表示可能是新奇策略对待 AA。

英文摘要：

Our previous studies have demonstrated that arsenic triox- ide （ATO） had the clinical efficacy in treating patients with aplastic anemia （AA）. However, the mechanisms remain to be elucidated. The important components of the bone marrow hematopoietic microenvironment, bone marrow mesenchymal stem cells （BMSCs）, are often altered in AA patients. In this study, it was found that AA BMSCs were prone to be induced into adipocytes rather than osteoblasts. ATO treatment can at least partially restore the differenti- ation imbalance of AA BMSCs. We further identified miR-204 as a key regulator in AA BMSC differentiation. Luciferase reporter assay showed that miR-204 could dir- ectly bind to the 3＇-untranslated region ofRunx2 mRNA, a key transcription factor regulating osteogenesis. Moreover, adipogenic differentiation was promoted and osteogenic differentiation was inhibited in miR-204 over-expressed cells, whereas osteogenesis was enhanced and adipocyte formation was inhibited in cells that lost miR-204 function, which suggested its endogenous function. Together we showed that ATO could inhibit adipogenic differentiation, but promote osteogenic differentiation in AA BMSCs, pro- viding a possible explanation for ATO clinical efficacy in AA patients. MiR-204 plays a key role in regulating BMSCs differentiation, and down-regulating miR-204 expression might be a novel strategy to treat AA.