ArticleArchives of medical research2014
Transcriptional profile of HIV-induced nuclear translocation of amyloid β in brain endothelial cells.
Article in Archives of medical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Functional impact of HIV-1 Tat on cells of the CNS and its role in HAND.Cellular and molecular life sciences : CMLS · 2020Review
- Extracellular vesicle-mediated amyloid transfer to neural progenitor cells: implications for RAGE and HIV infection.Molecular brain · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND AND
aimsIncreased amyloid deposition in HIV-infected brains may contribute to the pathogenesis of neurocognitive dysfunction in infected patients. We have previously shown that exposure to HIV results in enhanced amyloid β (Aβ) levels in human brain microvascular endothelial cells, suggesting that brain endothelial cells contribute to accumulation of Aβ in HIV-infected brains. Importantly, Aβ not only accumulates in the cytoplasm of HIV-exposed cells but also enters the nuclei of brain endothelial cells.
methodscDNA microarray analysis was performed in order to examine changes in the transcriptional profile associated with Aβ nuclear entry in the presence of HIV-1.
resultsGene network analysis indicated that inhibition of nuclear entry of Aβ resulted in enrichment in gene sets involved in apoptosis and survival, endoplasmic reticulum stress response, immune response, cell cycle, DNA damage, oxidative stress, cytoskeleton remodeling and transforming growth factor β (TGFβ) receptor signaling.
conclusionsThe obtained data indicate that HIV-induced Aβ nuclear uptake affects several cellular stress-related pathways relevant for HIV-induced Aβ pathology.
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