ArticleJournal of neuroinflammation2023
The novel HS-mimetic, Tet-29, regulates immune cell trafficking across barriers of the CNS during inflammation.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Antiviral Activity of Dendritic Heparan Sulfate Mimetics against Respiratory Syncytial Virus and Herpes Simplex Virus‑1.ACS omega · 2026Article
- Proteoglycan 4 attenuates ischemic post-stroke hemorrhagic transformation and blood-brain barrier disruption.IBRO neuroscience reports · 2025Article
- Nalmefene enhances the remyelinating ability of nalfurafine when administered therapeutically at very low doses during experimental autoimmune encephalomyelitis.Clinical & translational immunology · 2025Article
- Heparanase inhibition as a systemic approach to protect the endothelial glycocalyx and prevent microvascular complications in diabetes.Cardiovascular diabetology · 2024Article
- A charged tail on anti-α-Synuclein antibodies does not enhance their affinity to α-Synuclein fibrils.PloS one · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundDisruption of the extracellular matrix at the blood-brain barrier (BBB) underpins neuroinflammation in multiple sclerosis (MS). The degradation of extracellular matrix components, such as heparan sulfate (HS) proteoglycans, can be prevented by treatment with HS-mimetics through their ability to inhibit the enzyme heparanase. The heparanase-inhibiting ability of our small dendrimer HS-mimetics has been investigated in various cancers but their efficacy in neuroinflammatory models has not been evaluated. This study investigates the use of a novel HS-mimetic, Tet-29, in an animal model of MS.
methodsNeuroinflammation was induced in mice by experimental autoimmune encephalomyelitis, a murine model of MS. In addition, the BBB and choroid plexus were modelled in vitro using transmigration assays, and migration of immune cells in vivo and in vitro was quantified by flow cytometry.
resultsWe found that Tet-29 significantly reduced lymphocyte accumulation in the central nervous system which, in turn, decreased disease severity in experimental autoimmune encephalomyelitis. The disease-modifying effect of Tet-29 was associated with a rescue of BBB integrity, as well as inhibition of activated lymphocyte migration across the BBB and choroid plexus in transwell models. In contrast, Tet-29 did not significantly impair in vivo or in vitro steady state-trafficking under homeostatic conditions.
conclusionsTogether these results suggest that Tet-29 modulates, rather than abolishes, trafficking across central nervous system barriers.
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