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iTRAQ‐Based Proteomic Analysis Reveals Protein Profile in Plasma from Children with Autism
Author(s) -
Shen Liming,
Zhang Kaoyuan,
Feng Chengyun,
Chen Youjiao,
Li Shuiming,
Iqbal Javed,
Liao Liping,
Zhao Yuxi,
Zhai Jian
Publication year - 2018
Publication title -
proteomics – clinical applications
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.948
H-Index - 54
eISSN - 1862-8354
pISSN - 1862-8346
DOI - 10.1002/prca.201700085
Subject(s) - autism , pathophysiology , autism spectrum disorder , biology , medicine , endocrinology , psychiatry
Purpose Autism is a childhood neurological disorder with poorly understood etiology and pathology. This study is designed to identify differentially expressed proteins that might serve as potential biomarkers for autism. Experimental design We perform iTRAQ (isobaric tags for relative and absolute quantitation) analysis for normal and autistic children's plasma of the same age group. Results The results show that 24 differentially expressed proteins were identified between autistic subjects and controls. For the first time, differential expression of complement C5 (C5) and fermitin family homolog 3 (FERMT3) are related to autism. Five proteins, that is, complement C3 (C3), C5, integrin alpha‐IIb (ITGA2B), talin‐1 (TLN1), and vitamin D‐binding protein (GC) were validated via enzyme‐linked immunosorbent assay (ELISA). By ROC (receiver operating characteristic) analysis, combinations of these five proteins C3, C5, GC, ITGA2B, and TLN1 distinguished autistic children from healthy controls with a high AUC (area under the ROC curve) value (0.982, 95% CI, 0.957–1.000, p < 0.000). Conclusion These above described proteins are found involved in different pathways that have previously been linked to the pathophysiology of autism spectrum disorders (ASDs). The results strongly support that focal adhesions, acting cytoskeleton, cell adhesion, motility and migration, synaptogenesis, and complement system are involved in the pathogenesis of autism, and highlight the important role of platelet function in the pathophysiology of autism.