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

Abstract 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.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title biomed research international
Publication Year Start




PMID- 28251161
OWN - NLM
STAT- MEDLINE
DA  - 20170302
DCOM- 20170313
LR  - 20170313
IS  - 2314-6141 (Electronic)
VI  - 2017
DP  - 2017
TI  - Serum Proteome Alterations in Patients with Cognitive Impairment after Traumatic 
      Brain Injury Revealed by iTRAQ-Based Quantitative Proteomics.
PG  - 8572509
LID - 10.1155/2017/8572509 [doi]
AB  - 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.
FAU - Xiong, Xin-Gui
AU  - Xiong XG
AUID- ORCID: 0000-0002-8782-6563
AD  - Institute of Integrated Medicine, Xiangya Hospital, Central South University,
      Changsha, Hunan 410008, China.
FAU - Liang, Qinghua
AU  - Liang Q
AD  - Institute of Integrated Medicine, Xiangya Hospital, Central South University,
      Changsha, Hunan 410008, China.
FAU - Zhang, Chunhu
AU  - Zhang C
AD  - Institute of Integrated Medicine, Xiangya Hospital, Central South University,
      Changsha, Hunan 410008, China.
FAU - Wang, Yang
AU  - Wang Y
AUID- ORCID: 0000-0002-1225-6017
AD  - Institute of Integrated Medicine, Xiangya Hospital, Central South University,
      Changsha, Hunan 410008, China.
FAU - Huang, Wei
AU  - Huang W
AD  - Institute of Integrated Medicine, Xiangya Hospital, Central South University,
      Changsha, Hunan 410008, China.
FAU - Peng, Weijun
AU  - Peng W
AUID- ORCID: 0000-0002-4506-0942
AD  - Department of Integrated Traditional Chinese & Western Medicine, The Second
      Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
FAU - Wang, Zhe
AU  - Wang Z
AUID- ORCID: 0000-0002-1118-9721
AD  - Department of Integrated Traditional Chinese & Western Medicine, The Second
      Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
FAU - Xia, Zi-An
AU  - Xia ZA
AUID- ORCID: 0000-0002-0794-2960
AD  - Department of Integrated Traditional Chinese & Western Medicine, The Second
      Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
LA  - eng
PT  - Journal Article
DEP - 20170130
PL  - United States
TA  - Biomed Res Int
JT  - BioMed research international
JID - 101600173
RN  - 0 (Proteome)
SB  - IM
MH  - Adult
MH  - Brain Injuries, Traumatic/*blood/*complications
MH  - Cognition Disorders/*blood/*etiology
MH  - Demography
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Gene Ontology
MH  - Humans
MH  - Isotope Labeling/*methods
MH  - Male
MH  - Protein Interaction Mapping
MH  - Proteome/*metabolism
MH  - Proteomics/*methods
MH  - Reproducibility of Results
MH  - Signal Transduction
PMC - PMC5303854
COI - The authors declare that they have no competing interests.
EDAT- 2017/03/03 06:00
MHDA- 2017/03/14 06:00
CRDT- 2017/03/03 06:00
PHST- 2016/10/03 [received]
PHST- 2016/12/01 [revised]
PHST- 2016/12/13 [accepted]
AID - 10.1155/2017/8572509 [doi]
PST - ppublish
SO  - Biomed Res Int. 2017;2017:8572509. doi: 10.1155/2017/8572509. Epub 2017 Jan 30.

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