Defining Apolipoprotein-mediated Regulatory Pathways in Asthmatic Airways

我们利用屋尘螨诱导的哮喘小鼠模型来鉴定肺载脂蛋白E -低密度脂蛋白（LDL）受体通路作为气道高反应性和杯状细胞增生的内源性负调节因子（载脂蛋白E通过LDL受体介导的途径负调节屋尘螨诱导的哮喘）。姚鑫，Fredriksson K，余志新，徐鑫，Raghavachari N, Keeran KJ, Zywicke GJ, Kwak M, Amar MJ, Remaley AT, Levine SJ。Am J呼吸危重症护理医学2010年7月9日。印刷前的Epub)。这确定了一种新的机制，其中屋尘螨诱发哮喘的发病机制是调节的。正在进行的实验利用候选apoE-LDLR信号通路中候选基因缺失的小鼠，进一步确定apoE-LDLR信号负向调节哮喘气道高反应性和杯状细胞增生的机制。

We have utilized a murine model of house dust mite-induced asthma to identify that an apolipoprotein E - low density lipoprotein (LDL) receptor pathway in the lung functions as an endogenous negative regulator of airway hyperreactivity and goblet cell hyperplasia (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). This identified a novel mechanism by which the pathogenesis of house dust mite-induced asthma is modulated. Ongoing experiments are utilizing mice with deletions of candidate genes in candidate apoE-LDLR signaling pathways to define further the mechanisms by which apoE-LDLR signaling negatively regulates airway hyperreactivity and goblet cell hyperplasia in asthma.