Differential proteome analysis of bone marrow mesenchymal stem cells from adolescent idiopathic scoliosis patients.
Differential proteome analysis of bone marrow mesenchymal stem cells from adolescent idiopathic scoliosis patients.
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青少年特发性脊柱侧凸患者骨髓间充质干细胞的差异蛋白质组分析
DOI：
10.1371/journal.pone.0018834
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发表时间：
2011-04-22
期刊：
影响因子：
3.7
通讯作者：
Qiu G
中科院分区：
文献类型：
--
作者：
Zhuang Q;Li J;Wu Z;Zhang J;Sun W;Li T;Yan Y;Jiang Y;Zhao RC;Qiu G
青少年特发性脊柱侧凸（AIS）是一种复杂的三维脊柱畸形。尽管数十年的广泛研究，脊柱侧凸及其伴随的全身性骨质减少的病因和发病机制仍不清楚。本研究利用双向荧光差异凝胶电泳（2D-DIGE）结合质谱（MS）技术对AIS患者骨髓间充质干细胞（BM-MSCs）的差异蛋白质组进行分析。总共检测到41个显著改变的蛋白质点，其中34个点通过MALDI-TOF/TOF分析鉴定，并发现代表25种不同的基因产物。在这些蛋白质中，发现与骨生长和发育相关的五种蛋白质，包括丙酮酸激酶M2、膜联蛋白A2、热休克27 kDa蛋白、γ-肌动蛋白和β-肌动蛋白，被发现失调，因此选择用于通过Western印迹分析进一步验证。在蛋白水平上，我们的结果支持了先前的假设，即MSC的成骨分化能力下降是导致AIS骨质减少的机制之一。总之，我们首次分析了AIS患者的差异BM-MSCs蛋白质组，这可能有助于阐明AIS中骨丢失的潜在分子机制，并增加对AIS病因和发病机制的理解。
Adolescent idiopathic scoliosis (AIS) is a complex three-dimensional deformity of the spine. The cause and pathogenesis of scoliosis and the accompanying generalized osteopenia remain unclear despite decades of extensive research. In this study, we utilized two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) coupled with mass spectrometry (MS) to analyze the differential proteome of bone marrow mesenchymal stem cells (BM-MSCs) from AIS patients. In total, 41 significantly altered protein spots were detected, of which 34 spots were identified by MALDI-TOF/TOF analysis and found to represent 25 distinct gene products. Among these proteins, five related to bone growth and development, including pyruvate kinase M2, annexin A2, heat shock 27 kDa protein, γ-actin, and β-actin, were found to be dysregulated and therefore selected for further validation by Western blot analysis. At the protein level, our results supported the previous hypothesis that decreased osteogenic differentiation ability of MSCs is one of the mechanisms leading to osteopenia in AIS. In summary, we analyzed the differential BM-MSCs proteome of AIS patients for the first time, which may help to elucidate the underlying molecular mechanisms of bone loss in AIS and also increase understanding of the etiology and pathogenesis of AIS.
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