ArticleJournal of nanobiotechnology2023
Comparative study of extracellular vesicles derived from mesenchymal stem cells and brain endothelial cells attenuating blood-brain barrier permeability via regulating Caveolin-1-dependent ZO-1 and Claudin-5 endocytosis in acute ischemic stroke.
Article in Journal of nanobiotechnology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 2 of them syntheses that pooled it.
What it found
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Who cites it
85 citing papers in PubMed, 2 syntheses or guidelines pooled it, 123 citations in OpenAlex.
- Neuroimaging evidence of acupuncture in cognitive impairment following ischemic stroke: a systematic review.Frontiers in neuroscience · 2025Pooled it
- Stem cell-derived exosomes for ischemic stroke: a conventional and network meta-analysis based on animal models.Frontiers in pharmacology · 2024Pooled it
- Bone marrow-derived mesenchymal stem cells for ischemic stroke: mechanisms, delivery strategies, clinical evidence, and translational challenges.Stem cell research & therapy · 2026Review
- Mechanism-First Psychobiotics: Fermented Vegetables, Dairy, and Soy for Depression and Anxiety.International journal of molecular sciences · 2026Review
- Bone marrow mesenchymal stem cells protect against cerebral amyloid angiopathy by enhancing neutrophil mitocytosis.Neural regeneration research · 2026Article
- Targeting CD4⁺ T cell infiltration: mechanisms and therapeutic insights into CD4⁺ T cell transmigration across the blood-brain barrier in acute ischemic stroke.Fluids and barriers of the CNS · 2026Review
- PLAUR Exacerbates Neuroinflammation in Diabetic Ischemic Stroke by Driving Neutrophil-Mediated Blood-Brain Barrier Disruption and Reprogramming Microglial Metabolism.Neuromolecular medicine · 2026Article
- The Mechanistic Review of the Molecular Interface of RNA-Loaded Extracellular Vesicles: Redefining Targeted Therapy for Autoimmune Disorders.International journal of molecular sciences · 2026Review
- Targeting caveolin-1: dual challenges in tumor immunity and drug therapy strategies.Cancer cell international · 2026Review
- RVG-Modified BMSCs-Derived Small Extracellular Vesicles Loaded With miR-21 Alleviate Neuronal Injury Resulted From Excessive Autophagy via Targeting PTEN/Akt/mTOR Pathway After Cerebral Ischaemia.Journal of extracellular vesicles · 2026Article
- Extracellular vesicles: Revolutionizing targeted therapy for ischemic stroke.Acta pharmaceutica Sinica. B · 2026Review
- Targeted exosome-delivered CD151 siRNA maintains brain endothelial cell immune homeostasis to alleviate blood-brain barrier disruption after ischemic stroke.Journal of nanobiotechnology · 2026Article
- Cerebral Infarction: Epidemiology, Classification, Mechanisms, Diagnosis, and Management.MedComm · 2026Review
- Microfluidic-mass spectrometry analysis of blood-brain barrier transport using engineered microparticle interfaces.Chemical science · 2026Article
- BM-derived mesenchymal stem cell microvesicles protect enteric neural precursor cells and alleviate diabetes-associated enteric neuropathy.The Journal of clinical investigation · 2026Article
- Chemokine Networks in Blood-Brain Barrier Regulation: Bidirectional Mechanisms, Clinical Translation, and Precision Therapeutic Prospects.Biomolecules · 2026Review
- Endocytic Adaptor Proteins in Vascular Diseases: Critical Role of Intracellular Trafficking in Regulating Pathobiology of Vascular Disorders.Cardiology discovery · 2026Review
- Therapeutic potential of stem cell-derived extracellular vesicles in aging and regeneration.Frontiers in aging · 2026Review
- Harnessing extracellular vesicles for ischemic stroke management.Regenerative biomaterials · 2026Review
- Occludin-mediated barrier dysfunction and its role in cardiovascular and cerebrovascular pathogenesis.Frontiers in cardiovascular medicine · 2026Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundBlood-brain barrier (BBB) disruption is a major adverse event after ischemic stroke (IS). Caveolin-1 (Cav-1), a scaffolding protein, played multiple roles in BBB permeability after IS, while the pros and cons of Cav-1 on BBB permeability remain controversial. Numerous studies revealed that extracellular vesicles (EVs), especially stem cells derived EVs, exerted therapeutic efficacy on IS; however, the mechanisms of BBB permeability needed to be clearly illustrated. Herein, we compared the protective efficacy on BBB integrity between bone marrow mesenchymal stem cells derived extracellular vesicles (BMSC-EVs) and EVs from brain endothelial cells (BEC-EVs) after acute IS and investigated whether the mechanism was associated with EVs antagonizing Cav-1-dependent tight junction proteins endocytosis.
methodsBMSC-EVs and BEC-EVs were isolated and characterized by nanoparticle tracking analysis, western blotting, and transmission electron microscope. Oxygen and glucose deprivation (OGD) treated b. End3 cells were utilized to evaluate brain endothelial cell leakage. CCK-8 and TRITC-dextran leakage assays were used to measure cell viability and transwell monolayer permeability. Permanent middle cerebral artery occlusion (pMCAo) model was established, and EVs were intravenously administered in rats. Animal neurological function tests were applied, and microvessels were isolated from the ischemic cortex. BBB leakage and tight junction proteins were analyzed by Evans Blue (EB) staining and western blotting, respectively. Co-IP assay and Cav-1 siRNA/pcDNA 3.1 vector transfection were employed to verify the endocytosis efficacy of Cav-1 on tight junction proteins.
resultsBoth kinds of EVs exerted similar efficacies in reducing the cerebral infarction volume and BBB leakage and enhancing the expressions of ZO-1 and Claudin-5 after 24 h pMCAo in rats. At the same time, BMSC-EVs were outstanding in ameliorating neurological function. Simultaneously, both EVs treatments suppressed the highly expressed Cav-1 in OGD-exposed b. End3 cells and ischemic cerebral microvessels, and this efficacy was more prominent after BMSC-EVs administration. Cav-1 knockdown reduced OGD-treated b. End3 cells monolayer permeability and recovered ZO-1 and Claudin-5 expressions, whereas Cav-1 overexpression aggravated permeability and enhanced the colocalization of Cav-1 with ZO-1 and Claudin-5. Furthermore, Cav-1 overexpression partly reversed the lower cell leakage by BMSC-EVs and BEC-EVs administrations in OGD-treated b. End3 cells.
conclusionsOur results demonstrated that Cav-1 aggravated BBB permeability in acute ischemic stroke, and BMSC-EVs exerted similar antagonistic efficacy to BEC-EVs on Cav-1-dependent ZO-1 and Claudin-5 endocytosis. BMSC-EVs treatment was superior in Cav-1 suppression and neurological function amelioration.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.