Lackey Bernadette, Nunes Quentin M, Higham Susan M, Fernig David G, Valappil Sabeel P
Department of Health Services Research and School of Dentistry, University of Liverpool, Research Wing, Daulby Street, Liverpool, L69 3GN, UK.
NIHR Liverpool Pancreas Biomedical Research Unit, Royal Liverpool University Hospital, Daulby Street, Liverpool, L69 3GA, UK.
BMC Res Notes. 2016 Jan 28;9:53. doi: 10.1186/s13104-016-1857-1.
Periodontitis is described as a group of inflammatory diseases of the gingiva and supporting structures of the periodontium. The accumulation of plaque bacteria, which include putative periodontal pathogens, is known to initiate the disease but the host immune response is the major contributing factor for destruction of periodontal tissues. Proteins that bind to heparin heparin-binding protein (HBPs) play important roles in health and disease and interact with each other via networks known as 'heparin interactomes'. This study aimed at evaluating published datasets of HBPs and its role in periodontitis.
To elucidate the role of HBPs in periodontitis, bioinformatics analyses of published data was used. In silico analyses of published datasets were used to construct a putative HBPs interactome using an online database resource, 'STRING' (Search Tool for the Retrieval of Interacting Genes).
PubMed searches identified 249 genes that were up regulated and 146 genes that were down regulated in periodontal disease, compared with periodontal disease-free gingival samples. In silico analyses using published datasets revealed 25 up-regulated and 23 down-regulated HBPs in periodontitis. Of these HBPs; chemokines, such as CXCL12 was up regulated where as some of the matrixmetalloproteinases (MMPs; MMP-2 and MMP9) were up-regulated while MMP-14 was down regulated.
The results indicate that HBP analyses will provide multiple targets for the biological mechanisms underlying periodontal disease (such as MMPs, cytokines and chemokines) that will have important clinical implications in the future drug design and management of periodontal disease.
牙周炎被描述为一组牙龈及牙周支持组织的炎症性疾病。已知包括假定牙周病原体在内的菌斑细菌的积累会引发该疾病,但宿主免疫反应是牙周组织破坏的主要促成因素。与肝素结合的蛋白质——肝素结合蛋白(HBPs)在健康和疾病中发挥重要作用,并通过被称为“肝素相互作用组”的网络相互作用。本研究旨在评估已发表的HBPs数据集及其在牙周炎中的作用。
为阐明HBPs在牙周炎中的作用,对已发表的数据进行了生物信息学分析。利用在线数据库资源“STRING”(检索相互作用基因的搜索工具)对已发表的数据集进行计算机分析,以构建假定的HBPs相互作用组。
与无牙周疾病的牙龈样本相比,PubMed搜索确定在牙周疾病中有249个基因上调,146个基因下调。利用已发表的数据集进行的计算机分析显示,在牙周炎中有25个上调的HBPs和23个下调的HBPs。在这些HBPs中,趋化因子如CXCL12上调,而一些基质金属蛋白酶(MMPs;MMP - 2和MMP9)上调,而MMP - 14下调。
结果表明,HBP分析将为牙周疾病的生物学机制(如MMPs、细胞因子和趋化因子)提供多个靶点,这将对未来牙周疾病的药物设计和管理具有重要的临床意义。