Research Fields

 复杂性疾病易感基因的定位与克隆

 慢性炎症性疾病的分子发病机理

 动物模型的构建和评价

Customization(Multiple times)

 国家自然科学基金重点项目2项、国家自然科学基金项目6

PNEC-ILC2细胞单元的代谢重编程介导支气管哮喘的机制研究;

关节免疫炎症时特异SLC38A调节巨噬细胞活化的分子机制;

围孕期微营养素干预对先天性心脏病发生的一级预防作用及其机制;(重点项目

肺固有细胞中组蛋白修饰酶对哮喘气道重塑的作用机制研究;

蛋白质精氨酸甲基转移酶在哮喘中的作用机制研究;

PIA 模型大鼠Toll 样受体基因表达增高的分子机制研究;

大骨节病病因及发病机制研究;(重点项目

NOCIA大鼠模型筛选和鉴定类风湿关节炎的易感基因

 

 博士点基金项目1项春晖计划项目2项、“留学回国人员科研启动基金”1项、陕西省国际科技合作重点项目1项

降植烷诱导自噬参与免疫调节的分子机制研究;

先天性免疫细胞和分子及其在炎症中作用的分子机理;

Annexin I对NOCIA大鼠的影响及其影响机制的研究;

用大鼠模型鉴定类风湿关节炎的易感基因

以慢性免疫性疾病为对象,开展“疾病-基因-药物”的研究

Customization(Multiple times)

①创建了支气管哮喘的动物模型—AIPI,检测了肺脏和脾脏的PRMTs 表达谱,确定了PRMT1是调控AIPI 发生发展的一种关键表观遗传修饰酶,IL-4可通过诱导PRMT1 表达升高及其下游趋化因子的表达和分泌参与AIPI的发病机制;

 

②通过对降植烷诱导的关节炎(PIA)的TLR筛选,及进一步的TLR 配体刺激、RNAi 等动物实验及细胞实验确定巨噬细胞和滑膜成纤维细胞中高表达的TLR3对PIA 发生发展具有重要调控作用,其表达可受到 miRNA26a的负调控;

 

③通过近交系E3大鼠构建了高脂饮食诱导的胰岛素抵抗(HFD-IR)模型,发现其肝脏中HDAC3表达显著上调,上调的HDAC3可与sumo 化的C/EBPα结合负性调控LXRα表达;发现了一条新lnc-RNA,命名为lnc-HC,参与胆固醇的代谢;

 

④通过Solexa 方法获得大鼠骨软骨发育microRNA 表达谱,发现23种miRNA 显著高调,6 种miRNA 显著低调,及86 个新miRNA 的基因座位、序列和表达谱;进一步研究显示miR-337通过靶基因TGFBR2 作用于TGF-β 通路,从而参与调节软骨的生成及发育。

Customization(Multiple times)

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