ArticleJournal of neuroinflammation2018
Effect of tryptase on mouse brain microvascular endothelial cells via protease-activated receptor 2.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Mast cell proteases and their significance in physiology, pathology, and therapeutic approaches.Pharmacological reviews · 2026Review
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- Investigating Properties of Palmitoylethanolamide in Physiology and Disease: Far Beyond an Anti-Inflammatory Shield.Diseases (Basel, Switzerland) · 2026Review
- The Role of Mast Cells and Their Potential as a Therapeutic Target For Neuroinflammation.Journal of inflammation research · 2026Review
- Innate immune sensors and regulators at the blood brain barrier: focus on toll-like receptors and inflammasomes as mediators of neuro-immune crosstalk and inflammation.Journal of neuroinflammation · 2025Review
- Specific Mode Electroacupuncture Stimulation Mediates the Delivery of NGF Across the Hippocampus Blood-Brain Barrier Through p65-VEGFA-TJs to Improve the Cognitive Function of MCAO/R Convalescent Rats.Molecular neurobiology · 2025Article
- Mast cell-neuron axis as a core mechanism in chronic pruritus of atopic dermatitis: from mechanistic insights to therapeutic targets.Frontiers in immunology · 2025Review
- Role and mechanisms of mast cells in brain disorders.Frontiers in immunology · 2024Review
- TLR7 promotes smoke-induced experimental lung damage through the activity of mast cell tryptase.Nature communications · 2023Article
- Review
- Article
- SARS-CoV-2 productively infects human brain microvascular endothelial cells.Journal of neuroinflammation · 2022Article
- Protease-activated receptor-2 activation enhances epithelial wound healing via epidermal growth factor receptor.Tissue barriers · 2022Article
- Immunologic aspects of migraine: A review of literature.Frontiers in neurology · 2022Review
- Parenchymal neuroinflammatory signaling and dural neurogenic inflammation in migraine.The journal of headache and pain · 2021Review
- Article
- Inhibition of PAR-2 Attenuates Neuroinflammation and Improves Short-Term Neurocognitive Functions Via ERK1/2 Signaling Following Asphyxia-Induced Cardiac Arrest in Rats.Shock (Augusta, Ga.) · 2020Article
- Aloin Protects Against Blood-Brain Barrier Damage After Traumatic Brain Injury in Mice.Neuroscience bulletin · 2020Article
- Inhibition of mast cell tryptase attenuates neuroinflammation via PAR-2/p38/NFκB pathway following asphyxial cardiac arrest in rats.Journal of neuroinflammation · 2020Article
- Mast Cell Deficiency Protects Mice from Surgery-Induced Neuroinflammation.Mediators of inflammation · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMast cells (MCs), the 'first responders' in brain injury, are able to disrupt the blood-brain barrier (BBB), but the underlying mechanism is not well understood. Tryptase is the most abundant MC secretory product. Protease-activated receptor 2 (PAR-2) has been identified as a specific receptor for tryptase, which is abundantly expressed in brain microvascular endothelial cells. The BBB comprises brain microvascular endothelial cells that display specialised molecular properties essential for BBB function and integrity. Therefore, the purpose of the present study was to investigate the effects of tryptase on mouse brain microvascular endothelial cell line bEnd3 and its potential mechanisms of action.
methodsInduction of mouse brain microvascular endothelial cell activation by tryptase was examined. Then, mouse brain microvascular endothelial cells were pretreated with a PAR-2 antagonist and stimulated with tryptase. Cellular activation, proinflammatory cytokine production, expression of PAR-2, Toll-like receptors (TLRs) and mitogen-activated protein kinases (MAPK), nuclear factor kappa B (NF-kappa B) phosphorylation were assessed.
resultsTryptase upregulated the production of VCAM-1, MMPs (MMP9 and MMP2), TLR4 and TNF-α and downregulated the expression of the tight junction proteins occludin and claudin-5 in mouse brain microvascular endothelial cell. Among the MAPK and NF-kappa B pathway, ERK and NF-kappa B were activated by tryptase. All of these effects could be eliminated by the PAR-2 inhibitor.
conclusionBased on our findings, we conclude that tryptase can trigger brain microvascular endothelial cell activation and proinflammatory mediator release. These findings may further clarify the involvement and mechanism of tryptase in BBB disruption.
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