oxLDL- - -microRNA-155- - -MAP3K10途径反馈调控动脉粥样硬化免疫炎症反应的机制研究

在前期对miR-155功能研究的工作基础上，进一步突破传统的研究模式，围绕miR-155向上游和下游发散，抓住miR-155对靶基因MAP3K10的作用内在机制及miR-155本身如何被oxLDL调控的机制这两条主线进行深入研究，形成oxLDL-miR-155-MAP3K10反馈作用通路，观察miR-155 调控靶基因MAP3K10的作用位点及方式以及oxLDL下游各级炎症通路包括MAPK信号通路调控miR-155启动子的位点及作用方式，深入探讨miR-155通过MAP3K10调控AS免疫炎症病理过程中内在机制，为microRNA在动脉粥样硬化免疫炎症反应中的作用机制提供全新的认识，希望对AS发病机理、诊断、预后及疗效判定等多方面的研究起到推动作用, 同时申报国家发明专利，形成具有我国自主知识产权的学术成果。

On the basic of the previously work for the functional role of miR-155, focus on the miR-155 itself , then spread to upstream and downstream, we investigate these mechanisms are involved in the miR-155 regulation with atherosclerosis immune-inflammtory by target MAP3K10 and oxLDL-induced miR-155 upregulation .Our experiments first demonstrated the binding mechanism including the bingding site between miR-155 and MAP3K10, then further identified the mechanism of oxLDL-mediated microRNA-155 overexpression involved in oxLDL and its downstream signaling pathway of MAPK . Our findings can identify a novel feedback regulation between oxLDL, miR-155 and MAP3K10, and indicate that miR-155 could be a target to treat atherosclerosis.