Department of Biological Science and Engineering, Maulana Azad National Institute of Technology (MANIT), Bhopal, 462003, India.
Interdiscip Sci. 2018 Sep;10(3):500-514. doi: 10.1007/s12539-017-0213-z. Epub 2017 Mar 13.
Vitiligo is an idiopathic disorder characterized by depigmented patches on the skin due to progressive loss of melanocytes. Several genetic, immunological, and pathophysiological investigations have established vitiligo as a polygenetic disorder with multifactorial etiology. However, no definite model explaining the interplay between these causative factors has been established hitherto. Therefore, we studied the disorder at the system level to identify the key proteins involved by exploring their molecular connectivity in terms of topological parameters. The existing research data helped us in collating 215 proteins involved in vitiligo onset or progression. Interaction study of these proteins leads to a comprehensive vitiligo map with 4845 protein nodes linked with 107,416 edges. Based on centrality measures, a backbone network with 500 nodes has been derived. This has presented a clear overview of the proteins and processes involved and the crosstalk between them. Clustering backbone proteins revealed densely connected regions inferring major molecular interaction modules essential for vitiligo. Finally, a list of top order proteins that play a key role in the disease pathomechanism has been formulated. This includes SUMO2, ESR1, COPS5, MYC, SMAD3, and Cullin proteins. While this list is in fair agreement with the available literature, it also introduces new candidate proteins that can be further explored. A subnetwork of 64 vitiligo core proteins was built by analyzing the backbone and seed protein networks. Our finding suggests that the topology, along with functional clustering, provides a deep insight into the behavior of proteins. This in turn aids in the illustration of disease condition and discovery of significant proteins involved in vitiligo.
白癜风是一种特发性疾病,其特征是由于黑素细胞的进行性丧失,导致皮肤出现色素脱失斑块。多项遗传、免疫和病理生理学研究已经证实白癜风是一种多基因疾病,具有多因素病因。然而,迄今为止,尚未建立明确的模型来解释这些致病因素之间的相互作用。因此,我们在系统水平上研究该疾病,通过探索拓扑参数方面的分子连接性,确定涉及的关键蛋白。现有的研究数据帮助我们整理了 215 种与白癜风发病或进展有关的蛋白。对这些蛋白的相互作用研究导致了一个全面的白癜风图谱,图谱包含 4845 个蛋白节点和 107416 条边。基于中心度度量,从图谱中提取出一个包含 500 个节点的骨干网络。该骨干网络呈现了涉及的蛋白和过程及其相互作用的清晰概述。骨干蛋白聚类揭示了主要的分子相互作用模块,这些模块对于白癜风至关重要。最后,列出了在疾病发病机制中起关键作用的顶级蛋白列表,其中包括 SUMO2、ESR1、COPS5、MYC、SMAD3 和 Cullin 蛋白。虽然这个列表与现有文献基本一致,但它也引入了一些新的候选蛋白,可以进一步探索。通过分析骨干网络和种子蛋白网络构建了一个包含 64 个白癜风核心蛋白的子网络。我们的研究结果表明,拓扑结构以及功能聚类为深入了解蛋白的行为提供了深刻的见解。这反过来又有助于阐明疾病状况和发现与白癜风相关的重要蛋白。