Th2型细胞因子IL-4、IL-13是哮喘气道炎症反应的关键因子，VEGF是关键的血管生成促进因子，在哮喘的气道炎症和气道重塑中起到重要作用。生物信息学软件预测miR-410存在与IL-4、IL-13、VEGF 的结合位点；我们前期实验发现miR-410能够负性调节ova诱导哮喘小鼠气道IL-4、IL-13 细胞因子的表达，减轻哮喘小鼠模型的气道炎症反应，提示miR-410可能是治疗哮喘气道炎症的新靶点。本课题拟通过双荧光素酶报告基因明确miR-410靶向VEGF、IL-4、IL-13的作用；观察其对肺微血管内皮细胞增殖、粘附、渗透性及VEGF表达的调控作用；进一步观察其对CD4+T分泌IL-4、IL-13直接调控作用；最后在动物实验方面验证miR-410对OVA诱导哮喘小鼠模型气道炎症及气道重塑的影响。本研究有助阐明哮喘发病的分子机制，为临床哮喘的治疗发现新靶点提供理论和实验依据。

Th2 cytokines, like IL-4, IL-13 are key points of asthma inflammation of airway while vascular endothelial growth factor (VEGF) plays an important role in airway remodeling of asthma. A series of bioinformatics software were applied and found that miR-410 could target and bind VEGF,IL-4,IL-13 mRNA 3’UTR. Our previous study showed that miR-410 negatively regulates the expression of IL-4 and IL-13 in BALF of asthma and could also suppress inflammatory response of airway in OVA sensitized asthma murine model. These findings suggest that miR-410 plays an important role in regulation of airway inflammaion and might be involved in the pathogenesis underlying asthma. In the current study, we will determine whether or not miR-410 targets VEGF,IL-4,IL-13mRNA. In vitro, we will elaberate if miR-410 has a negative regulation for expression of IL-4,IL-13 from CD4+T cells and if it could regulate proliferation, adhesion and permeability of pulmonary microvascular endothelial cells by VEGF. Then, we will determine the effect of miR-410 on OVA sensitized airway inflammation, pulmonary vascular permeability to elucidate the role of miR-410 in the pathogenesis of OVA sensitized asthma. This research will help to clarify the molecular mechanism involved in asthma and provide a theoretical and experimental basis for the discovery of new targets for the clinical treatment of asthma.