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De-regulation of diabetic regulatory genes in psoriasis: Deciphering the unsolved riddle

机译:牛皮癣中糖尿病调节基因的失调:破译未解之谜

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The purpose of our study was to identify the currently lacking molecular mechanism that accounts for the co-occurrence of two seemingly disparate diseases: psoriasis and type II diabetes. We aimed to investigate a panel of 84 genes related to the diabetic regulatory network in psoriasis (Ps), psoriasis type II diabetes (Ps-T2D), type II diabetes (T2D) and healthy control (HC). We hypothesize that such attempts would provide novel diagnostic markers and/or insights into pathogenesis of the disease. A quantitative Real Time-PCR Human Diabetes RT2 Profiler PCR Array was chosen to explore the expression profile 84 diabetic genes in study subjects. Statistical analysis was carried out using appropriate software. The analysis revealed three candidate genes GSK3B, PTPN1, STX4 that are differentially expressed in study subjects. GSK3B was highly significant in Ps-T2D (P = 0.00018, FR = -26.6), followed by Ps (P = 0.0028, FR = -14.5) and T2D groups (P = 0.032, FR = -5.9). PTPN1 showed significant association only with PS-T2D (P = 0.00027, FR = -8.5). STX4 showed significant association with both Ps (P = 0.0002, FR = -20) and Ps-T2D (P = 0.0016, FR = -11.2). ACE represents an additional marker that showed suggestive association with Ps (P = 0.0079, FR = -9.37). Our study highlights the complex genetics of Ps-T2D and present biomarkers for the development of T2D in Ps cases. (C) 2016 Published by Elsevier B.V.
机译:我们研究的目的是确定目前缺乏的分子机制来解释两种看似截然不同的疾病:银屑病和II型糖尿病。我们旨在研究与银屑病(Ps),II型银屑病(Ps-T2D),II型糖尿病(T2D)和健康对照(HC)的糖尿病调节网络相关的84个基因。我们假设这样的尝试将为疾病的发病机理提供新颖的诊断标记和/或见解。选择定量实时PCR-人类糖尿病RT2 Profiler PCR Array来研究研究对象中84个糖尿病基因的表达情况。使用适当的软件进行统计分析。分析揭示了三个候选基因GSK3B,PTPN1,STX4在研究对象中差异表达。 GSK3B在Ps-T2D(P = 0.00018,FR = -26.6)中非常重要,其次是Ps(P = 0.0028,FR = -14.5)和T2D组(P = 0.032,FR = -5.9)。 PTPN1仅与PS-T2D显示显着关联(P = 0.00027,FR = -8.5)。 STX4显示与Ps(P = 0.0002,FR = -20)和Ps-T2D(P = 0.0016,FR = -11.2)均显着相关。 ACE代表显示与Ps暗示关联的其他标记(P = 0.0079,FR = -9.37)。我们的研究突出了Ps-T2D的复杂遗传学,并为Ps病例中T2D的发展提供了生物标记。 (C)2016由Elsevier B.V.发布

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