ArticleExperimental cell research2014
HIV-1 stimulates nuclear entry of amyloid beta via dynamin dependent EEA1 and TGF-β/Smad signaling.
Article in Experimental cell research, 2014. 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, 16 citations in OpenAlex.
- Host Genetic Regulation of NLRP3 Inflammasome Cytokines Reveals Immune and Vascular Pathways in HIV.medRxiv : the preprint server for health sciences · 2026Article
- Differential Blood-Brain Barrier Transport and Cell Uptake of Cyclic Peptides In Vivo and In Vitro.Pharmaceutics · 2023Article
- Suppression of TGF-β/Smad2 signaling by GW788388 enhances DENV-2 clearance in macrophages.Journal of medical virology · 2022Article
- HIV-1 and Amyloid Beta Remodel Proteome of Brain Endothelial Extracellular Vesicles.International journal of molecular sciences · 2020Article
- Extracellular vesicle-mediated amyloid transfer to neural progenitor cells: implications for RAGE and HIV infection.Molecular brain · 2020Article
- HIV Infection Induces Extracellular Cathepsin B Uptake and Damage to Neurons.Scientific reports · 2019Article
- 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
- HIV-1 Tat Regulates Occludin and Aβ Transfer Receptor Expression in Brain Endothelial Cells via Rho/ROCK Signaling Pathway.Oxidative medicine and cellular longevity · 2016Article
- Protective effects of calcitriol on diabetic nephropathy are mediated by down regulation of TGF-β1 and CIP4 in diabetic nephropathy rat.International journal of clinical and experimental pathology · 2015Article
- Transcriptional profile of HIV-induced nuclear translocation of amyloid β in brain endothelial cells.Archives of medical research · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Clinical evidence indicates increased amyloid deposition in HIV-1-infected brains, which contributes to neurocognitive dysfunction in infected patients. Here we show that HIV-1 exposure stimulates amyloid beta (Aβ) nuclear entry in human brain endothelial cells (HBMEC), the main component of the blood-brain barrier (BBB). Treatment with HIV-1 and/or Aβ resulted in concurrent increase in early endosomal antigen-1 (EEA1), Smad, and phosphorylated Smad (pSmad) in nuclear fraction of HBMEC. A series of inhibition and silencing studies indicated that Smad and EEA1 closely interact by influencing their own nuclear entry; the effect that was attenuated by dynasore, a blocker of GTP-ase activity of dynamin. Importantly, inhibition of dynamin, EEA1, or TGF-β/Smad effectively attenuated HIV-1-induced Aβ accumulation in the nuclei of HBMEC. The present study indicates that nuclear uptake of Aβ involves the dynamin-dependent EEA1 and TGF-β/Smad signaling pathways. These results identify potential novel targets to protect against HIV-1-associated dysregulation of amyloid processes at the BBB level.
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