ArticleFluids and barriers of the CNS2026
Endothelial tPA-dependent recruitment of microglia to vessels protects the blood-brain barrier after stroke.
Article in Fluids and barriers of the CNS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Friend or foe? Glial-vascular interactions in health and neurodegenerative disease.Pharmacological reviews · 2026Review
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5 authors.
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Abstract
backgroundIschemic stroke is one of the leading causes of death and disability worldwide and thrombolysis, with tissue-type plasminogen activator (tPA) or its mutants, remains the only pharmacological treatment available for the acute phase. In this study, we hypothesised that endothelial tPA plays a key role in modulating the microglial response and maintaining blood brain barrier (BBB) integrity after stroke.
methodsUsing a mouse model with endothelial-specific deletion of tPA (VeCad
resultsOur results demonstrate that microglia-vessel contacts increase post-stroke. Notably, deletion of endothelial tPA reduces vascular cell adhesion molecule 1 (VCAM1) expression and is associated with decreased microglial activation and fewer microglia-vessel contacts. Interestingly, endothelial tPA deletion also leads to increased BBB permeability and a heightened risk of haemorrhagic transformation following stroke.
conclusionsCollectively, these findings indicate that endothelial tPA promotes microglial recruitment to blood vessels and plays a protective role in preserving BBB integrity after ischemic stroke.
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