Heywood Wendy E, Bliss Emily, Mills Philippa, Yuzugulen Jale, Carreno Gabriela, Clayton Peter T, Muntoni Francesco, Worthington Viki C, Torelli Silvia, Sebire Neil J, Mills Kevin, Grunewald Stephanie
Centre for Inborn Errors of Metabolism, Great Ormond Street Hospital, Great Ormond Street, London WC1N 3JH, UK; Centre for Translational Omics, UCL Institute of Child Health & Great Ormond Street Hospital NHS Foundation Trust, London WC1N 1EH, UK.
Centre for Inborn Errors of Metabolism, Great Ormond Street Hospital, Great Ormond Street, London WC1N 3JH, UK.
Mol Genet Metab Rep. 2016 Apr 17;7:55-62. doi: 10.1016/j.ymgmr.2016.03.002. eCollection 2016 Jun.
The Congenital Disorders of Glycosylation (CDG) are an expanding group of genetic disorders which encompass a spectrum of glycosylation defects of protein and lipids, including N- & O-linked defects and among the latter are the muscular dystroglycanopathies (MD). Initial screening of CDG is usually based on the investigation of the glycoproteins transferrin, and/or apolipoprotein CIII. These biomarkers do not always detect complex or subtle defects present in older patients, therefore there is a need to investigate additional glycoproteins in some cases. We describe a sensitive 2D-Differential Gel Electrophoresis (DIGE) method that provides a global analysis of the serum glycoproteome. Patient samples from PMM2-CDG (n = 5), CDG-II (n = 7), MD and known complex N- & O-linked glycosylation defects (n = 3) were analysed by 2D DIGE. Using this technique we demonstrated characteristic changes in mass and charge in PMM2-CDG and in charge in CDG-II for α1-antitrypsin, α1-antichymotrypsin, α2-HS-glycoprotein, ceruloplasmin, and α1-acid glycoproteins 1&2. Analysis of the samples with known N- & O-linked defects identified a lower molecular weight glycoform of C1-esterase inhibitor that was not observed in the N-linked glycosylation disorders indicating the change is likely due to affected O-glycosylation. In addition, we could identify abnormal serum glycoproteins in LARGE and B3GALNT2-deficient muscular dystrophies. The results demonstrate that the glycoform pattern is varied for some CDG patients not all glycoproteins are consistently affected and analysis of more than one protein in complex cases is warranted. 2D DIGE is an ideal method to investigate the global glycoproteome and is a potentially powerful tool and secondary test for aiding the complex diagnosis and sub classification of CDG. The technique has further potential in monitoring patients for future treatment strategies. In an era of shifting emphasis from gel- to mass-spectral based proteomics techniques, we demonstrate that 2D-DIGE remains a powerful method for studying global changes in post-translational modifications of proteins.
糖基化先天性疾病(CDG)是一类不断扩大的遗传性疾病,涵盖了蛋白质和脂质糖基化缺陷的一系列情况,包括N-连接和O-连接缺陷,其中后者包括肌营养不良聚糖病(MD)。CDG的初步筛查通常基于对糖蛋白转铁蛋白和/或载脂蛋白CIII的检测。这些生物标志物并不总能检测出老年患者中存在的复杂或细微缺陷,因此在某些情况下需要研究其他糖蛋白。我们描述了一种灵敏的二维差异凝胶电泳(DIGE)方法,该方法可对血清糖蛋白组进行全面分析。通过二维DIGE分析了来自PMM2-CDG(n = 5)、CDG-II(n = 7)、MD以及已知复杂N-连接和O-连接糖基化缺陷(n = 3)的患者样本。使用该技术,我们证明了在PMM2-CDG中α1-抗胰蛋白酶、α1-抗糜蛋白酶、α2-HS-糖蛋白、铜蓝蛋白以及α1-酸性糖蛋白1和2的质量和电荷发生了特征性变化,在CDG-II中电荷发生了变化。对已知N-连接和O-连接缺陷的样本分析发现了一种分子量较低的C1酯酶抑制剂糖型,在N-连接糖基化疾病中未观察到,这表明这种变化可能是由于O-糖基化受到影响。此外,我们能够在LARGE和B3GALNT2缺陷型肌营养不良症中鉴定出异常血清糖蛋白。结果表明,一些CDG患者的糖型模式各不相同,并非所有糖蛋白都受到一致影响,在复杂病例中对多种蛋白质进行分析是必要的。二维DIGE是研究整体糖蛋白组的理想方法,是辅助CDG复杂诊断和亚分类的潜在有力工具和二次检测方法。该技术在监测患者未来治疗策略方面具有进一步的潜力。在一个从基于凝胶的蛋白质组学技术向基于质谱的蛋白质组学技术转变的时代,我们证明二维DIGE仍然是研究蛋白质翻译后修饰整体变化的有力方法。