lncRNA-MEG3-miRNA交互作用调控肾缺血后血管新生的研究

Restoring blood supply as soon as possible is the key point to prevent kidney injury after renal ischemia.Thus exploring the mechanism of angiogenesis for effective therapeutic measures is of great significance.Recent research indicated that LncRNA-MEG3 is closely related to angiogenesis.LncRNA can interact with miRNA via binding microRNA response elements (MREs). In our preliminary study，through qRT-PCR, Microarrays technologies and combining bioinformatics analysis ,we found the expression level of lncRNA-MEG3, miRNA-Let-7e and its target gene changed remarkably after renal ischemia and these molecules shared a common MRE bingding site.We assumed that MEG3 and Let-7 may be involved in regulating angiogenesis after renal ischemia by cross action each other.In this study,we aim to investigate the role of MEG3,Let-7 and its target in the process of angiogenesis in response to renal ischemia injury and clarify the molecular regulation mechanisms on angiogenesis by cross action between lncRNA and miRNA after renal ischemia.

肾缺血发生后，促进缺血区血运重建，尽快恢复缺血肾组织的血供是防止肾功能损伤的关键,因此深入探讨血管新生的机制为治疗性血管新生寻找有效治疗靶点具有重要意义。近来有证据表明lncRNA-MEG3与血管新生过程密切相关；对lncRNA作用机制的最新研究发现lncRNA可通过miRNA应答元件（MRE）与miRNA交互作用调控转录后基因表达。我们前期研究通过qRT-PCR，基因芯片及生物信息学技术分析发现肾缺血后MEG3与miRNA-let-7e及其靶基因发生明显变化，并且二者存在相同MRE，我们分析MEG3极有可能通过与let-7e交互调控参与肾缺血后血管新生过程。本项目拟在前期研究基础上，进一步通过体内外实验深入探讨MEG3、Let-7及其靶基因在肾缺血后血管新生过程中的作用及调控关系，明确lncRNA-miRNA交互作用调控血管新生的功能和途径，以期进一步揭示肾缺血后血管新生的调控机制。