Comparative study of serum proteomes in Legg-Calve-Perthes disease

BMC Musculoskeletal Disorders

Chuanyi Bai²  Hang Gao¹  Xiaoqian Dang²  Qichun Song²  Wusheng Miao³  Kunzheng Wang²  Longbin Yin²  Lihong Fan²  Ruiyu Liu² 

[1] Research Center for Proteome Analysis, Shanghai Institutes for Biological5 Sciences, Chinese Academy of Sciences, Shanghai, P. R China;Department of Orthopaedic, the Second Hospital Affilicated to Medical College, Xi’an Jiaotong University, No.157, Xiwu Road, Xi’an 710004, Shaanxi, P. R China;Department of Pediatric Orthopaedic, Hong-Hui Hospital, Medical College of Xi’an Jiaotong University, No. 76 Nanguo Road, Nanshao Men, Beilin District, Xi’an 710054, P. R China

关键词: Lipid metabolism;    Isobaric tags for relative and absolute quantification;    Serum proteome;    Legg-Calve-Perthes disease;   

Others  :  1232895
DOI  :  10.1186/s12891-015-0730-z

 received in 2015-02-24, accepted in 2015-09-21,  发布年份 2015

【 摘 要 】

Background

Legg-Calve-Perthes Disease (LCPD) is an idiopathic osteonecrosis of the developing femoral head complicated by pain and disability of the hip joint. To date, the pathological mechanisms of LCPD are not well-known. This study screened the changes in serum protein expression in patients with LCPD.

Methods

Age- and sex-matched serum samples from 10 control subjects and 10 patients with LCPD were compared using the isobaric tags for relative and absolute quantification (iTRAQ) technique. Gene ontology analyses, KEGG pathway and functional network analyses were performed. Proteins of interest with large differences in expression, S100-A8, alpha-1-acid glycoprotein 1, haptoglobin and apolipoprotein E, were compared by western blotting.

Results

The disease/control ratios showed 26 proteins were significantly differentially expressed (all p < 0.05). Including higher abundances of complement factor H (1.44), complement C4-B (1.45), isocitrate dehydrogenase [NAD] subunit alpha (2.7) alpha-1-acid glycoprotein 1 (1.87), heptoglobin (1.53) and Ig lambda-2 chain C regions (1.46), and lower levels of apolipoprotein E (0.50), apolipoprotein F (0.60), apolipoprotein C-III (0.69), S100-A8 (0.73), S100-A9 (0.75) and prothrombin (0.77) in LCPD than in controls. The alpha-1-acid glycoprotein 1 and haptoglobin increases, and apolipoprotein E and S100-A8 decreases were confirmed by western blot. KEGG pathway analysis revealed these proteins were related to the complement and coagulation cascades, Staphylococcus aureus infection, PPAR signaling, fat digestion and absorption, and vitamin digestion and absorption. Functional network analysis suggested that the proteins were involved in lipid regulation.

Conclusions

The complement and coagulation cascades, and abnormal lipid metabolism may be involved in the pathogenesis of LCPD.

【 授权许可】

   
2015 Liu et al.

【 图 表 】

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