| First Author | Searcy JL | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 2 | Pages | e89970 |
| PubMed ID | 24587158 | Mgi Jnum | J:214476 |
| Mgi Id | MGI:5603024 | Doi | 10.1371/journal.pone.0089970 |
| Citation | Searcy JL, et al. (2014) Impact of age on the cerebrovascular proteomes of wild-type and Tg-SwDI mice. PLoS One 9(2):e89970 |
| abstractText | The structural integrity of cerebral vessels is compromised during ageing. Abnormal amyloid (Abeta) deposition in the vasculature can accelerate age-related pathologies. The cerebrovascular response associated with ageing and microvascular Abeta 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 Abeta 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. |
