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Proteomics Analysis of Myocardial Tissues in a Mouse Model of Coronary Microembolization

机译:冠状微栓塞小鼠模型中心肌组织的蛋白质组学分析

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摘要

Coronary microembolization (CME) is an important clinical problem, and it is related to poor outcome. The specific molecular mechanisms of CME are not fully understood. In the present study, we established a mice model of CME. Isobaric tags for relative and absolute quantitation (iTRAQ) and liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) technologies identified 249 differentially expressed proteins in the myocardial tissues of CME mice as compared with sham-operated mice. Bioinformatics analysis demonstrated that these differentially expressed proteins were enriched in several energy metabolism or cytoskeleton organization related processes or pathways. Quantitative PCR and Western blotting validation experiments revealed that succinate dehydrogenase (SDHA and SDHB) were upregulated, Rho GDP dissociation inhibitor α (RhoGDIα) and Filamin-A (FLNA) were downregulated significantly in CME mice. These findings indicated that the alternations of the cytoskeleton and energy metabolism pathways play important roles in the pathogenesis of CME, future studies are warranted to verify if targeting these molecules might be useful to alleviate CME injury or not.
机译:冠状动脉微栓塞术(CME)是一个重要的临床问题,与不良预后有关。 CME的具体分子机制尚未完全了解。在本研究中,我们建立了CME的小鼠模型。相对和绝对定量(iTRAQ)的等压标签以及液相色谱与串联质谱(LC-MS / MS)技术相结合,与假手术小鼠相比,在CME小鼠的心肌组织中鉴定出249种差异表达的蛋白质。生物信息学分析表明,这些差异表达的蛋白质富含几种能量代谢或细胞骨架组织相关的过程或途径。定量PCR和Western印迹验证实验表明,在CME小鼠中琥珀酸脱氢酶(SDHA和SDHB)被上调,Rho GDP解离抑制剂α(RhoGDIα)和Filamin-A(FLNA)被显着下调。这些发现表明,细胞骨架和能量代谢途径的改变在CME的发病机理中起着重要的作用,因此有必要进行进一步的研究以验证靶向这些分子是否有助于缓解CME损伤。

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