ArticleMicrocirculation (New York, N.Y. : 1994)2025
Regulation of BzATP-Induced Blood-Brain Barrier Endothelial Cell Hyperpermeability by NLRP3 Inflammasome Inhibition.
Article in Microcirculation (New York, N.Y. : 1994), 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Article
- Tau Oligomers Induce Brain Endothelial Cell Hyperpermeability and Increase NLRP3 Inflammasome Signaling and MMP-9 Activity.Microcirculation (New York, N.Y. : 1994) · 2026Article
- Targeting the blood-brain barrier with phytochemicals to attenuate vascular cognitive impairment: mechanisms and therapeutic potential across etiologies.Frontiers in nutrition · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
objectiveThe blood-brain barrier (BBB) is a semi-permeable microvascular barrier, composed of endothelial cells conjoined by tight junction proteins. Following pathological conditions, i.e., traumatic brain injury (TBI), BBB dysfunction occurs, leading to microvascular hyperpermeability, resulting in cerebral edema formation and elevated intracranial pressure. Recent evidence suggests that the activation of pro-inflammatory signaling pathways is critical to BBB dysfunction. The NLRP3 inflammasome has been implicated as a key component of pro-inflammatory signaling. The aim of this study was to determine the upstream regulators of NLRP3 inflammasome activation that cause subsequent BBB aberration and microvascular hyperpermeability.
methodsBrain microvascular endothelial cells were exposed to benzoyl ATP (BzATP) with or without MCC950. We employed immunocytochemical localization of tight junction proteins, fluorometric enzymatic assays, total gene expression analyses of ZO-1, and monolayer permeability studies to assess the effect of BzATP-induced injury on NLRP3 inflammasome activation/inhibition.
resultsBzATP treatment induced monolayer hyperpermeability and increased caspase-1 and MMP-9 activities. NLRP3 inhibition decreased caspase-1 and MMP-9 activities and rescued BzATP-induced monolayer permeability significantly.
conclusionsNLRP3 inflammasome signaling is critical to BBB endothelial cell dysfunction. Extracellular ATP is an upstream promoter of BBB hyperpermeability. NLRP3 inflammasome activation leads to subsequent caspase-1 and MMP-9-mediated tight junction protein disarray.
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