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Applying label‐free quantitative proteomics to identify profile protein changes in hippocampus of rats after chronic cerebral hypoperfusion
Author(s) -
Wang YueHua,
Yang YingLin,
Cheng Xiao,
Lyu Yang,
Du GuanHua
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.500.10
Subject(s) - hippocampus , hippocampal formation , medicine , vascular dementia , quantitative proteomics , phosphorylation , proteomics , neuroscience , bioinformatics , biology , dementia , microbiology and biotechnology , gene , biochemistry , disease
Vascular dementia (VD) refers to a progressive decline in memory and cognitive function caused by chronic cerebral hypoperfusion. 2‐vessels occlusion (2‐VO) induced by bilateral common carotid artery occlusion has been widely used as a model of VD. In the present study, the global proteins profile of hippocampus in 2‐VO rats was studied using label‐free quantitative proteomics. The results showed that 2‐VO induced learning and memory deficits, motor ability dysfunction, and neuronal plasticity injury in rats. The proteomics results showed that there are involved in up‐regulation of 55 proteins and down‐regulation of 171 proteins in the hippocampus of 2‐VO group vs that of sham group. Gene ontology and signal pathway analysis showed that the regulated proteins are mainly involved in intracellular signaling cascade, metabolic process, oxidation reduction process, oxidative phosphorylation, etc. Furthermore, RT‐PCR results revealed that the mRNA expression of Mt‐nd1, Serpine2, Mrpl15 was significantly decreased and whereas Itapka, Ptpn1, Abracl, Gorasp2 were significantly increased in the hippocampus of 2‐VO rats compared with sham rats. WB result further demonstrated MT‐ND1 expression was consistent with the results of proteomics. The current findings provide new insights into the molecular mechanisms of chronic cerebral ischemia. Support or Funding Information National Key Research and Development Program of China (2018YFC0311005), National Natural Science Foundation of China (81473383), National Science and Technology Major Project of China (2018ZX09711001‐003‐019), CAMS Innovation Fund for Medical Sciences (2016‐I2M‐3‐007), and Innovation Fund for Graduate of Beijing Union Medical College (2017‐1007‐02; 2018‐1007‐04). This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .