LOXL1与TGF-β相关分子作用路径的预测

Predicting Molecule Pathways between LOXL1 and TGF-β

摘要: 盆腔器官脱垂(POP)是一种盆底支持结构功能障碍性疾病，而现有的手术手段并不能根治这种疾病，因此探究POP的发病机制是一项比较有意义的研究。已有的资料表明，类氨酰氧化酶——LOXL1的敲除能够导致小鼠在分娩之后发生POP。同时TGF-β的表达量高低与POP的严重程度相关。在已经掌握资料的基础上，我们对网络上现有的海量微阵列数据进行了查找，选取了其中两个数据集进行分析。我们通过数据挖掘的方式对于POP相关的生物芯片进行相关性分析以及聚类，最后建立生物学网络。我们发现TGF-β同时通过smad与非smad通路调控LOXL1的表达，而LOXL1在细胞外基质参与黏着斑的形成、弹性纤维与胶原的交联等等。

Abstract: POP refers to a pelvic floor structure support disorder that visceras in the female pelvic cavity move down along its normal position. However, there is no radical cure for it. So it is a significant research to inquire the pathogenesis of POP. From the information already in hand, we know that LOXL1 knock-down mouse will always produce POP after delivery. In the meantime, the expression of TGF-β has a strong relationship with the severity of POP. On the basis of the data already known, we search for the massive data on the Internet and chose two data sets to do the analysis. As for data mining, we do correlation analysis and cluster on the microarrays that we had chosen. Finally, to show it more clearly, we set up a biology network. We found that TGF-β can regulate the expression of LOXL1 through the smad and non-smad pathways, meanwhile, LOXL1 is involved in the formation of focal adhesion and the crosslinking between elastin and collagen.