Characterizing the Role of Apolipoprotein Receptors in Asthma Pathogenesis

我们已经证实载脂蛋白E通过低密度脂蛋白受体(LDLR)依赖的机制(载脂蛋白E通过低密度脂蛋白受体介导的途径对屋尘螨诱导的哮喘进行负性调节)在哮喘的气道高反应性和杯状细胞增生中发挥内源性负性调节作用。姚X，弗雷德里克森·K，于正欣，徐翔，拉加瓦查里·N，基兰·KJ，Zywicke GJ，Kwak M，Amar MJ，Remaley AT，Levine SJ。Am J Respir CRUT CARE Med。2010年7月9日，印刷前的ePub)。载脂蛋白E是由肺内巨噬细胞合成的，其作用是通过与纤毛呼吸道上皮细胞上表达的LDLRs结合而介导的。该项目将利用载脂蛋白受体基因敲除小鼠来确定其他载脂蛋白受体在调节哮喘发病机制中的作用。此外，将描述肺载脂蛋白受体调节哮喘发病机制的机制。

We have identified that apolipoprotein E serves as an endogenous negative regulator of airway hyperreactivity and goblet cell hyperplasia in asthma by a low density lipoprotein receptor(LDLR)-dependent mechanism (Apolipoprotein E Negatively Regulates House Dust Mite-induced Asthma via a LDL Receptor-mediated Pathway. Yao X, Fredriksson K, Yu ZX, Xu X, Raghavachari N, Keeran KJ, Zywicke GJ, Kwak M, Amar MJ, Remaley AT, Levine SJ. Am J Respir Crit Care Med. 2010 Jul 9. Epub ahead of print). The effects of apoE, which is synthesized by macrophages in the lung, are mediated via binding to LDLRs that are expressed on ciliated airway epithelial cells. This project will utilize apolipoprotein receptor knock-out mice to define the role of other apolipoprotein receptors in modulating the pathogenesis of asthma. Furthermore, the mechanisms by which asthma pathogenesis is modulated by lung apolipoprotein receptors will be characterized.