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01.12.2015 | Research article | Ausgabe 1/2015 Open Access

BMC Musculoskeletal Disorders 1/2015

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

Zeitschrift:
BMC Musculoskeletal Disorders > Ausgabe 1/2015
Autoren:
Ruiyu Liu, Lihong Fan, Longbin Yin, Kunzheng Wang, Wusheng Miao, Qichun Song, Xiaoqian Dang, Hang Gao, Chuanyi Bai
Wichtige Hinweise

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

RYL, CYB, XQD and KZW Conceived and designed the experiments; LBY, HG and QCS performed the experiments and collected the serum sample; LHF, HG and QCS analyzed the data; RYL, CYB, LHF and LBY wrote the paper. All authors read and approved the final manuscript.

Authors’ information

Not applicable.

Abstract

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.
Literatur
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