Serum Proteome Alterations in Patients with Cognitive Impairment after Traumatic Brain Injury Revealed by iTRAQ-Based Quantitative Proteomics

• Published in: BioMed research international Vol. 2017; no. 2017; pp. 1 - 13
• Main Authors: Xia, Zian, Peng, Weijun, Huang, Wei, Wang, Yang, Zhang, Chunhu, Liang, Qinghua, Xiong, Xin-Gui, Wang, Zhe
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01.01.2017; Hindawi; John Wiley & Sons, Inc
• Subjects: Adult; Brain; Brain Injuries, Traumatic - blood; Brain Injuries, Traumatic - complications; Cognition disorders; Cognition Disorders - blood; Cognition Disorders - etiology; Cognitive ability; Demography; Development and progression; Disease; Enzyme-Linked Immunosorbent Assay; Female; Gene Ontology; Health care; Hospitals; Humans; Injuries; Isotope Labeling - methods; Male; Medical research; Medicine, Experimental; Protein Interaction Mapping; Proteins; Proteome - metabolism; Proteomics; Proteomics - methods; Reproducibility of Results; Risk factors; Signal Transduction; Studies; Traumatic brain injury
• ISSN: 2314-6133; 2314-6141; 2314-6141
• DOI: 10.1155/2017/8572509

Background. Cognitive impairment is the leading cause of traumatic brain injury- (TBI-) related disability; however, the underlying pathogenesis of this dysfunction is not completely understood. Methods. Using an isobaric tagging for relative and absolute quantitation- (iTRAQ-) based quantitative proteomic approach, serum samples from healthy control subjects, TBI patients with cognitive impairment, and TBI patients without cognitive impairment were analysed to identify differentially expressed proteins (DEPs) related to post-TBI cognitive impairment. In addition, DEPs were further analysed using bioinformatic platforms and validated using enzyme-linked immunosorbent assays (ELISA). Results. A total of 56 DEPs were identified that were specifically related to TBI-induced cognitive impairment. Bioinformatic analysis revealed that a wide variety of cellular and metabolic processes and some signaling pathways were involved in the pathophysiology of cognitive deficits following TBI. Five randomly selected DEPs were validated using ELISA in an additional 105 cases, and the results also supported the experimental findings. Conclusions. Despite limitations, our findings will facilitate further studies of the pathological mechanisms underlying TBI-induced cognitive impairment and provide new methods for the research and development of neuroprotective agents. However, further investigation on a large cohort is warranted.