Sabaouni Imane, Vannier Brigitte, Moussa Ahmed, Ibrahimi Azeddine
Medical Biotechnology Lab (MedBiotech), Rabat Medical & Pharmacy School, Mohammed Vth University in Rabat, Morocco.
Receptors, Regulation and Tumor Cells (2RTC) Laboratory, University of Poitiers, France.
Bioinformation. 2016 Oct 11;12(6):332-339. doi: 10.6026/97320630012332. eCollection 2016.
CD36 is a multifunctional membrane-type receptor glycoprotein that reacts with oxidized low-density lipoprotein and long-chain fatty acid (LCFA). However, much remains to be understood about the molecular mechanism of the cardio-myopathy observed in CD36-KO mice. In this study, we identify different genes pathways involved in response to CD36 cardio-myopathy phenotype by identifying the differences among biological processes, molecular pathways and networks of interactions that emerge from knocking CD3 and using different bioinformatics tools such as STRING, GeneMANIA and Cytoscape. We were able list all the CD36-regulated genes, their related function and their specific networks. Data analysis showed that CD36-regulated genes differentially expressed are involved in biological processes such as FA metabolism, angiogenesis/apoptosis and cell structure. These results provide the first look at mechanisms involved in CD36 deficiency and development of cardio-myopathy and the opportunity to identify new therapeutic targets.
CD36是一种多功能膜型受体糖蛋白,可与氧化型低密度脂蛋白和长链脂肪酸(LCFA)发生反应。然而,关于在CD36基因敲除(KO)小鼠中观察到的心肌病的分子机制,仍有许多有待了解之处。在本研究中,我们通过识别敲除CD36后出现的生物学过程、分子途径和相互作用网络之间的差异,并使用STRING、GeneMANIA和Cytoscape等不同的生物信息学工具,确定了参与应对CD36心肌病表型的不同基因途径。我们能够列出所有受CD36调控的基因、它们的相关功能及其特定网络。数据分析表明,差异表达的受CD36调控的基因参与脂肪酸代谢、血管生成/凋亡和细胞结构等生物学过程。这些结果首次揭示了CD36缺乏与心肌病发生机制,并为识别新的治疗靶点提供了机会。