ArticleScientific reports2019
HIV Infection Induces Extracellular Cathepsin B Uptake and Damage to Neurons.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 34 citations in OpenAlex.
- HIV Tat-activated microglial extracellular vesicles induce neuronal iron dysregulation and synaptodendritic injury.Cell communication and signaling : CCS · 2026Article
- Cathepsin B protease mediates high population density-induced mutagenesis to drive genome evolution and competitive growth.Nature communications · 2026Article
- Extracellular vesicle dysfunction contributes to synaptic and cognitive deficits in a mouse model of Angelman syndrome.Progress in neurobiology · 2026Article
- Cysteine protease cathepsin B promotes high population density-induced mutagenesis, driving genome evolution and competitive growth in response to the crowding stress.bioRxiv : the preprint server for biology · 2025Article
- Inflammatory microglia signals drive A1-like polarization of astrocytes even in the presence of HIV-1 Tat.Molecular neurobiology · 2025Article
- Cannabinoid Receptor Type 2 Agonist JWH-133 Stimulates Antiviral Factors and Decreases Proviral, Inflammatory, and Neurotoxic Proteins in HIV-Infected Macrophage Secretome.International journal of molecular sciences · 2025Article
- Analysis of Sigma-1 Receptor Antagonist BD1047 Effect on Upregulating Proteins in HIV-1-Infected Macrophages Exposed to Cocaine Using Quantitative Proteomics.Biomedicines · 2024Article
- Quantitative Proteomics Reveal That CB2R Agonist JWH-133 Downregulates NF-κB Activation, Oxidative Stress, and Lysosomal Exocytosis from HIV-Infected Macrophages.International journal of molecular sciences · 2024Article
- Role of microglia in HIV-1 infection.AIDS research and therapy · 2023Review
- Decreased CSTB, RAGE, and Axl Receptor Are Associated with Zika Infection in the Human Placenta.Cells · 2022Article
- Extralysosomal cathepsin B in central nervous system: Mechanisms and therapeutic implications.Brain pathology (Zurich, Switzerland) · 2022Review
- Neurodegenerative phagocytes mediate synaptic stripping in Neuro-HIV.Brain : a journal of neurology · 2022Article
- Molecular Features of CA-074 pH-Dependent Inhibition of Cathepsin B.Biochemistry · 2022Article
- Inhibition of Cathepsin B and SAPC Secreted by HIV-Infected Macrophages Reverses Common and Unique Apoptosis Pathways.Journal of proteome research · 2022Article
- Cannabinoid receptor type 2 agonist JWH-133 decreases cathepsin B secretion and neurotoxicity from HIV-infected macrophages.Scientific reports · 2022Article
- Bromodomains in Human-Immunodeficiency Virus-Associated Neurocognitive Disorders: A Model of Ferroptosis-Induced Neurodegeneration.Frontiers in neuroscience · 2022Review
- High cathepsin A protein expression predicts poor prognosis and tumor recurrence of hepatocellular carcinoma patients after curative hepatectomy.American journal of cancer research · 2022Article
- Extracellular Vesicles and HIV-Associated Neurocognitive Disorders: Implications in Neuropathogenesis and Disease Diagnosis.Neurotoxicity research · 2021Review
- The Role of Extracellular Vesicles from Human Macrophages on Host-Pathogen Interaction.International journal of molecular sciences · 2021Review
- Alzheimer's-Like Pathology at the Crossroads of HIV-Associated Neurological Disorders.Vaccines · 2021Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
HIV-associated neurocognitive disorders prevail in 20-50 percent of infected individuals. Macrophages transmigrate through the blood brain barrier during HIV-1 infection, triggering neuronal dysfunction. HIV-infected macrophages secrete cathepsin B (CATB), and serum amyloid p component (SAPC), inducing neuronal apoptosis by an unknown mechanism. We hypothesized that HIV infection facilitates CATB/SAPC secretion from macrophages followed by neuronal internalization, promoting dysfunction. SK-N-SH neuronal cells were exposed to active recombinant histidine-tagged cathepsin B (His-CATB). His-CATB entry was tracked by intracellular flow cytometry, and neuronal dysfunction was verified by western blot. Macrophage-derived extracellular vesicles (EVs) were tested for the presence of CATB and SAPC. Neurons internalized His-CATB, an effect that was partially decreased by pre-treatment with anti-CATB antibody. Pre-treatment with CATB and SAPC antibodies decreased cleavage of caspase-3 and restored synaptophysin in neurons. Neurons exposed to macrophage-conditioned media differentially internalized His-CATB, dependent on the HIV replication levels. Finally, CATB and SAPC were secreted in EVs. We report for the first time that CATB is secreted from macrophages both free and in EVs, and is internalized by neurons. Moreover, HIV-replication levels modulate the amount of CATB neuronal uptake, and neuronal dysfunction can be decreased with CATB antibodies. In conclusion, the CATB/SAPC complex represents a novel target against HIV-associated neurocognitive disorders.
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