期刊
PLOS ONE
卷 9, 期 2, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0089970
关键词
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资金
- Alzheimer Society [1742]
- Alzheimer's Research UK
- SynthSys
- BBSRC
- EPSRC [BB/D019621/1]
- AXA Research Fund
- BBSRC [BB/D019621/1] Funding Source: UKRI
- Alzheimers Research UK [ART-PG2010-3] Funding Source: researchfish
- Biotechnology and Biological Sciences Research Council [BB/D019621/1] Funding Source: researchfish
The structural integrity of cerebral vessels is compromised during ageing. Abnormal amyloid (Ab) deposition in the vasculature can accelerate age-related pathologies. The cerebrovascular response associated with ageing and microvascular Ab deposition was defined using quantitative label-free shotgun proteomic analysis. Over 650 proteins were quantified in vessel-enriched fractions from the brains of 3 and 9 month-old wild-type (WT) and Tg-SwDI mice. Sixty-five proteins were significantly increased in older WT animals and included several basement membrane proteins (nidogen-1, basement membrane-specific heparan sulfate proteoglycan core protein, laminin subunit gamma-1 precursor and collagen alpha-2(IV) chain preproprotein). Twenty-four proteins were increased and twenty-one decreased in older Tg-SwDI mice. Of these, increases in Apolipoprotein E (APOE) and high temperature requirement serine protease-1 (HTRA1) and decreases in spliceosome and RNA-binding proteins were the most prominent. Only six shared proteins were altered in both 9-month old WT and Tg-SwDI animals. The age-related proteomic response in the cerebrovasculature was distinctly different in the presence of microvascular A beta deposition. Proteins found differentially expressed within the WT and Tg-SwDI animals give greater insight to the mechanisms behind age-related cerebrovascular dysfunction and pathologies and may provide novel therapeutic targets.
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