ArticleProceedings of the National Academy of Sciences of the United States of America2025
Vamp3/syntaxin 4 mediates the basolateral membrane fusion of TfR transcytosis across the BBB and is exploited by pathogenic
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Targeting VAMPs in Aging-Related Diseases: From Mechanisms to Pharmacotherapy.Pharmaceutical research · 2026Review
- Liver-nervous system axis: pathways, dysregulation, and translational perspectives.Journal of neuroinflammation · 2026Review
- Extracellular vesicle therapeutics in Alzheimer's disease: mechanisms, progress, and prospects.Extracellular vesicles and circulating nucleic acids · 2026Review
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Authors and funding
12 authors.
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Abstract
Transcytosis across the blood-brain barrier (BBB), composed of brain microvascular endothelial cells (HBMECs), is tightly controlled to prevent the entry of macromolecules, microorganisms, and toxins into the brain. Transferrin receptor (TfR) transcytosis, one of the few active transcytosis pathways in HBMECs, is extensively utilized for drug transport across the BBB and employed by meningitis-causing bacteria to penetrate into the brain. However, the molecular mechanism facilitating the fusion of TfR vesicles with the basolateral membrane of HBMECs, the final step of transcytosis, has not been experimentally studied. Here, we found that the interaction between the v-SNARE protein VAMP3 on TfR vesicles and the t-SNARE protein syntaxin 4 that is limited to the basolateral membrane in HBMECs mediates the fusion. We also provided evidence that this step is critical for the efficiency of TfR transcytosis. Furthermore, we showed that neonatal meningitis
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