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Blue native/SDS-PAGE combined with iTRAQ analysis reveals advanced glycation end-product-induced changes of synaptosome proteins in C57 BL/6 mice.

Authors
  • Xie, Chunliang
  • Liu, Nvying
  • Long, Jia
  • Tang, Cheng
  • Li, Jianglin
  • Huo, Linju
  • Wang, Xianchun
  • Chen, Ping
  • Liang, Songping
Type
Published Article
Journal
Electrophoresis
Publisher
Wiley (John Wiley & Sons)
Publication Date
Aug 01, 2011
Volume
32
Issue
16
Pages
2194–2205
Identifiers
DOI: 10.1002/elps.201100125
PMID: 21792995
Source
Medline
License
Unknown

Abstract

Evidence shows that administration of high-level D-galactose induces the production of advanced glycation end-products (AGEs) that have been implicated in the development of diabetic complications such as neuropathy. The deterioration of learning and memory during neuropathy might be associated with the altered expression of proteins in synapse. To evaluate AGE-induced protein network alterations in synapse, blue native/SDS-PAGE and iTRAQ proteomic methods were used to screen for differentially expressed synaptic proteins of cerebral cortex in D-galactose-induced C57 BL/6 mice. In total, the expression level of 84 proteins is changed during AGE accumulation. The significantly differentially expressed proteins mainly participate in neurotransmission, energy metabolism and signal transduction pathway, suggesting that energy metabolism is damaged and neurotransmission is attenuated in synapse. The results of in vivo activities of malondialdehyde and superoxide dismutase suggested that AGE accumulation in the brain leads to the generation of reactive oxygen species. Therefore, elucidating the differentially expressed proteins underlying the AGE accumulation will open a new window to the mechanism of learning and memory impairments in neuropathy.

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