我们已发现流体剪切力（FSS）上调miR-20a的表达，并证明miR-20a介导了FSS诱导的成骨细胞分化。miR-20a上调的机制是什么？证据表明FSS激活了Smads。5'末端序列续减分析确立了诱导miR-20a表达的启动子核心区并发现一个Smads结合序列。miR-20a抑制哪些靶点起作用？分析提示miR-20a很可能抑制BMP2信号转导负调控因子BAMBI、Smad6及PPAR?。由此，我们首次提出：FSS激活Smads上调miR-20a，miR-20a抑制BAMBI、Smad6或PPAR?，最终激活BMP2信号并促进成骨细胞分化。本研究拟通过前期实验模型，应用RNA干扰、CALUX及CHIP技术，旨在获得Smads直接上调miR-20a及miR-20a激活BMP2信号的可靠证据，阐明miR-20a对FSS促成骨细胞分化的作用和机制，从而为机械刺激促牙槽骨改建补充新的理论和调控靶点

We had found that fluid shear stress (FSS) up-regulated the expression of miR-20a, and demonstrated that miR-20a mediated osteoblast differentiation induced by FSS. However, why miR-20a was up-regulated？ Further experiments showed that FSS phosphorylated Smads. A binding sequence with Smads in the miR-20a promoter core area was discovered by 5 'terminal sequence analysis. But which targets do miR-20a inhibited to promote osteoblast differentiation? The target genes of miR-20a included transduction negative regulator of BMP2 signal, such as BAMBI, Smad6, PPAR? and so on. Thus, we firstly proposed: FSS up-regulates miR-20a by Smads signal, miR-20a suppresses BAMBI, Smad6 or PPAR? and activates BMP2 signaling to promote osteoblast differentiation. This study is proposed to obtain reliable evidence that FSS up-regulates miR-20a by BMP2/Smads signal and miR-20a activates BMP2 signal, using the established experimental models and application of RNA interference, CALUX and CHIP technology. It is expected to demonstrate the function and mechanisms of miR-20a during osteoblast differentiation induced by FSS, so as to complement the new theory and regulatory targets for alveolar bone remodeling under mechanical stimulations.