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HIV-1 Tat-induced cerebrovascular toxicity is enhanced in mice with amyloid deposits.

Abstract：

:HIV-1-infected brains are characterized by elevated depositions of amyloid beta (Aβ); however, the interactions between Aβ and HIV-1 are poorly understood. In the present study, we administered specific HIV-1 protein Tat into the cerebral vasculature of 50-52-week-old double transgenic (B6C3-Tg) mice that express a chimeric mouse/human amyloid precursor protein (Mo/HuAPP695swe) and a mutant human presenilin 1 (PS1-dE9) and are characterized by increased Aβ depositions in the brain. Exposure to Tat increased permeability across cerebral capillaries, enhanced disruption of zonula occludens (ZO)-1 tight junction protein, and elevated brain expression of matrix metalloproteinase-9 (MMP-9) in B6C3-Tg mice as compared with age-matched littermate controls. These changes were associated with increased leukocyte attachment and their transcapillary migration. The majority of Tat-induced effects were attenuated by treatment with a specific Rho inhibitor, hydroxyfasudil. The results of animal experiments were reproduced in cultured brain endothelial cells exposed to Aβ and/or Tat. The present data indicate that increased brain levels of Aβ can enhance vascular toxicity and proinflammatory responses induced by HIV-1 protein Tat.

journal_name

Neurobiol Aging

journal_title

Neurobiology of aging

authors

Chen L,Choi JJ,Choi YJ,Hennig B,Toborek M

doi

10.1016/j.neurobiolaging.2011.06.004

subject

Has Abstract

pub_date

2012-08-01 00:00:00

pages

1579-90

issue

8

eissn

0197-4580

issn

1558-1497

pii

S0197-4580(11)00213-2

journal_volume

33

pub_type

杂志文章

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