ArticleBiochemical and biophysical research communications2012
Lipid rafts and functional caveolae regulate HIV-induced amyloid beta accumulation in brain endothelial cells.
Article in Biochemical and biophysical research communications, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Review
- Endocytic Pathways Unveil the Role of Syndecans in the Seeding and Spreading of Pathological Protein Aggregates: Insights into Neurodegenerative Disorders.International journal of molecular sciences · 2025Review
- Brain endothelium-derived extracellular vesicles containing amyloid-beta induce mitochondrial alterations in neural progenitor cells.Extracellular vesicles and circulating nucleic acids · 2022Article
- Alzheimer's-Like Pathology at the Crossroads of HIV-Associated Neurological Disorders.Vaccines · 2021Review
- Role of Cav-1 in HIV-1 Tat-Induced Dysfunction of Tight Junctions and AOxidative medicine and cellular longevity · 2019Article
- Extracellular vesicles of the blood-brain barrier: Role in the HIV-1 associated amyloid beta pathology.Molecular and cellular neurosciences · 2017Article
- HIV-1 Transactivator Protein Induces ZO-1 and Neprilysin Dysfunction in Brain Endothelial Cells via the Ras Signaling Pathway.Oxidative medicine and cellular longevity · 2017Article
- Transcriptional profile of HIV-induced nuclear translocation of amyloid β in brain endothelial cells.Archives of medical research · 2014Article
- HIV-1 stimulates nuclear entry of amyloid beta via dynamin dependent EEA1 and TGF-β/Smad signaling.Experimental cell research · 2014Article
- The hCMEC/D3 cell line as a model of the human blood brain barrier.Fluids and barriers of the CNS · 2013Article
- Amyloid beta accumulation in HIV-1-infected brain: The role of the blood brain barrier.IUBMB life · 2013Review
- Caveolins: targeting pro-survival signaling in the heart and brain.Frontiers in physiology · 2012Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Amyloid beta (Aβ) levels are increased in HIV-1 infected brains due to not yet fully understood mechanisms. In the present study, we investigate the role of lipid rafts, functional caveolae, and caveolae-associated signaling in HIV-1-induced Aβ accumulation in HBMEC. Both silencing of caveolin-1 (cav-1) and disruption of lipid rafts by pretreatment with beta-methyl-cyclodextrin (MCD) protected against Aβ accumulation in HBMEC. Exposure to HIV-1 and Aβ activated caveolae-associated Ras and p38. While inhibition of Ras by farnesylthiosalicylic acid (FTS) effectively protected against HIV-1-induced accumulation of Aβ, blocking of p38 did not have such an effect. We also evaluated the role of caveolae in HIV-1-induced upregulation of the receptor for advanced glycation end products (RAGE), which regulates Aβ transfer from the blood stream into the central nervous system. HIV-1-induced RAGE expression was prevented by infecting HBMEC with cav-1 specific shRNA lentiviral particles or by pretreatment of cells with FTS. Overall, the present results indicate that Aβ accumulation in HBMEC is lipid raft and caveolae dependent and involves the caveolae-associated Ras signaling.
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