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人亨廷顿病诱导多能干细胞的定量蛋白质组分析。

Quantitative proteomic analysis of induced pluripotent stem cells derived from a human Huntington's disease patient.

机构信息

Department of Oral Pharmacology, School of Dentistry and Institute of Dental Bioscience, BK21 project, Chonbuk National University, Jeonju 651-756, Korea.

出版信息

Biochem J. 2012 Sep 15;446(3):359-71. doi: 10.1042/BJ20111495.

Abstract

HD (Huntington's disease) is a devastating neurodegenerative genetic disorder caused by abnormal expansion of CAG repeats in the HTT (huntingtin) gene. We have recently established two iPSC (induced pluripotent stem cell) lines derived from a HD patient carrying 72 CAG repeats (HD-iPSC). In order to understand the proteomic profiles of HD-iPSCs, we have performed comparative proteomic analysis among normal hESCs (human embryonic stem cells; H9), iPSCs (551-8) and HD-iPSCs at undifferentiated stages, and identified 26 up- and down-regulated proteins. Interestingly, these differentially expressed proteins are known to be involved in different biological processes, such as oxidative stress, programmed cell death and cellular oxygen-associated proteins. Among them, we found that oxidative stress-related proteins, such as SOD1 (superoxide dismutase 1) and Prx (peroxiredoxin) families are particularly affected in HD-iPSCs, implying that HD-iPSCs are highly susceptible to oxidative stress. We also found that BTF3 (basic transcription factor 3) is up-regulated in HD-iPSCs, which leads to the induction of ATM (ataxia telangiectasia mutated), followed by activation of the p53-mediated apoptotic pathway. In addition, we observed that the expression of cytoskeleton-associated proteins was significantly reduced in HD-iPSCs, implying that neuronal differentiation was also affected. Taken together, these results demonstrate that HD-iPSCs can provide a unique cellular disease model system to understand the pathogenesis and neurodegeneration mechanisms in HD, and the identified proteins from the present study may serve as potential targets for developing future HD therapeutics.

摘要

HD(亨廷顿舞蹈症)是一种由 HTT(亨廷顿蛋白)基因中 CAG 重复异常扩增引起的毁灭性神经退行性遗传疾病。我们最近建立了两条源自携带 72 个 CAG 重复的 HD 患者的 iPSC(诱导多能干细胞)系(HD-iPSC)。为了了解 HD-iPSC 的蛋白质组学特征,我们在未分化阶段对正常 hESC(人胚胎干细胞;H9)、iPSC(551-8)和 HD-iPSC 进行了比较蛋白质组学分析,并鉴定出 26 个上调和下调的蛋白质。有趣的是,这些差异表达的蛋白质已知参与不同的生物学过程,如氧化应激、细胞程序性死亡和与细胞氧相关的蛋白质。其中,我们发现氧化应激相关的蛋白质,如 SOD1(超氧化物歧化酶 1)和 Prx(过氧化物酶)家族在 HD-iPSC 中受到特别影响,这意味着 HD-iPSC 对氧化应激非常敏感。我们还发现,BTF3(基本转录因子 3)在 HD-iPSC 中上调,导致 ATM(共济失调毛细血管扩张突变)的诱导,随后激活 p53 介导的凋亡途径。此外,我们观察到 HD-iPSC 中细胞骨架相关蛋白的表达显著降低,这意味着神经元分化也受到影响。综上所述,这些结果表明 HD-iPSC 可以提供一个独特的细胞疾病模型系统,以了解 HD 中的发病机制和神经退行性变机制,并且本研究中鉴定的蛋白质可能成为未来开发 HD 治疗方法的潜在靶点。

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