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Comparative analysis of serum proteomes of degenerative scoliosis
Author(s) -
Zhu Yong,
Han Shijie,
Zhao Hong,
Liang Jinqian,
Zhai Jiliang,
Wu Zhihong,
Qiu Guixing
Publication year - 2011
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1002/jor.21466
Subject(s) - clusterin , pathogenesis , proteome , biology , western blot , scoliosis , gene isoform , medicine , immunology , pathology , bioinformatics , gene , genetics , apoptosis
Degenerative scoliosis (DS) is an important degenerative lumbar disease causing spinal dysfunction and affecting the quality of life of the elderly, and is associated not only with severe back or leg pain but also with complicated surgical outcomes. The pathogenesis of DS is still unknown. Therefore, it is very important to ascertain the etiology of degenerative scoliosis and establish related molecular markers predicting and controlling the scoliosis. For the first time, we used two‐dimensional fluorescence DIGE to compare the serum proteome profiles of 12 DS patients and controls. Proteins found to be differentially expressed were identified by MALDI‐TOF mass spectrometric analysis, coupled with database interrogation. Eleven spots that were differentially expressed in the sera of DS patients were found, and eight gene products were identified among these spots. Clusterin, CLU cDNA FLJ57622, ALB cDNA FLJ50830, Hypothetical short protein, HLA‐A MHC class 1 antigen. (Fragment), ALB 23 kDa protein, Isoform 1 of G protein‐regulated inducer of neurite outgrowth 1 (GPRIN I)and Ficolin‐3 were down‐regulated in the sera of DS patients. The decreased levels of Clusterin and Ficolin‐3 were confirmed by Western blot. The information obtained with this proteomic analysis will be very useful in understanding the pathophysiology of DS as well as in finding candidates as drug targets of DS. These results may provide a novel approach for the pathogenesis study of DS. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 29:1896–1903, 2011