ArticleMolecular neurobiology2019
Canonical Wnt Pathway Maintains Blood-Brain Barrier Integrity upon Ischemic Stroke and Its Activation Ameliorates Tissue Plasminogen Activator Therapy.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Acupuncture improves blood-brain barrier integrity through multi-targeted mechanisms: a preclinical meta-analysis.Frontiers in neurology · 2025Pooled it
- Stress induces behavioral disorders by promoting microglial phagocytosis via decreasing neuronal Dkk3.Molecular psychiatry · 2025Article
- Electroacupuncture Potentiates Astragaloside IV Cerebral Delivery via P-Glycoprotein-Mediated Transcellular Transport: A Novel Blood-Brain Barrier Penetration Strategy for Ischemic Stroke Therapy.Brain and behavior · 2025Article
- VEGF-E Attenuates Injury After Ischemic Stroke by Promoting Reparative Revascularization.The European journal of neuroscience · 2025Article
- Ginsenoside Rb1 attenuates neuroflammation via activating Wnt/β-catenin signaling pathway to exert neuroprotective effect on cerebral ischemic-reperfusion injury.Frontiers in aging neuroscience · 2025Article
- Critical role of Slc22a8 in maintaining blood-brain barrier integrity after experimental cerebral ischemia-reperfusion.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025Article
- Unbiased quantification of the spatial distribution of murine cells using point pattern analysis.STAR protocols · 2024Article
- GPR124 regulates murine brain embryonic angiogenesis and BBB formation by an intracellular domain-independent mechanism.Development (Cambridge, England) · 2024Article
- Endothelial PDGF-D contributes to neurovascular protection after ischemic stroke by rescuing pericyte functions.Cellular and molecular life sciences : CMLS · 2024Article
- Tankyrase inhibition interferes with junction remodeling, induces leakiness, and disturbs YAP1/TAZ signaling in the endothelium.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Ischemia-reperfusion injury: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Non-classical monocytes promote neurovascular repair in cerebral small vessel disease associated with microinfarctions via CX3CR1.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- Regulation of the Blood-Brain Barrier in Health and Disease.Cold Spring Harbor perspectives in medicine · 2023Article
- Protocadherin gamma C3: a new player in regulating vascular barrier function.Neural regeneration research · 2023Review
- Intrinsic blood-brain barrier dysfunction contributes to multiple sclerosis pathogenesis.Brain : a journal of neurology · 2022Article
- Pharmacological suppression of glycogen synthase kinase-3 reactivates HIV-1 from latency via activating Wnt/β-catenin/TCF1 axis in CD4Emerging microbes & infections · 2022Article
- Stem Cell- and Cell-Based Therapies for Ischemic Stroke.Bioengineering (Basel, Switzerland) · 2022Review
- GLP-1R Agonist Exendin-4 Protects Against Hemorrhagic Transformation Induced by rtPA After Ischemic Stroke via the Wnt/β-Catenin Signaling Pathway.Molecular neurobiology · 2022Article
- RNA-Seq Profiling of Neutrophil-Derived Microvesicles in Alzheimer's Disease Patients Identifies a miRNA Signature That May Impact Blood-Brain Barrier Integrity.International journal of molecular sciences · 2022Article
- Hemorrhagic Transformation After Tissue Plasminogen Activator Treatment in Acute Ischemic Stroke.Cellular and molecular neurobiology · 2022Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Stroke induces blood-brain barrier (BBB) breakdown, which promotes complications like oedema and hemorrhagic transformation. Administration of recombinant tissue plasminogen activator (rtPA) within a therapeutic time window of 4.5 h after stroke onset constitutes the only existing treatment. Beyond this time window, rtPA worsens BBB breakdown. Canonical Wnt pathway induces BBB formation and maturation during ontogeny. We hypothesized that the pathway is required to maintain BBB functions after stroke; thus, its activation might improve rtPA therapy. Therefore, we first assessed pathway activity in the brain of mice subjected to transient middle cerebral artery occlusion (MCAo). Next, we evaluated the effect of pathway deactivation early after stroke onset on BBB functions. Finally, we assessed the impact of pathway activation on BBB breakdown associated to delayed administration of rtPA. Our results show that pathway activity is induced predominately in endothelial cells early after ischemic stroke. Early deactivation of the pathway using a potent inhibitor, XAV939, aggravates BBB breakdown and increases hemorrhagic transformation incidence. On the other hand, pathway activation using a potent activator, 6-bromoindirubin-3'-oxime (6-BIO), reduces the incidence of hemorrhagic transformation associated to delayed rtPA administration by attenuating BBB breakdown via promotion of tight junction formation and repressing endothelial basal permeability independently of rtPA proteolytic activity. BBB preservation upon pathway activation limited the deleterious effects of delayed rtPA administration. Our study demonstrates that activation of the canonical Wnt pathway constitutes a clinically relevant strategy to extend the therapeutic time window of rtPA by attenuating BBB breakdown via regulation of BBB-specific mechanisms.
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