ArticleJournal of cellular and molecular medicine2018
S1PR3 is essential for phosphorylated fingolimod to protect astrocytes against oxygen-glucose deprivation-induced neuroinflammation via inhibiting TLR2/4-NFκB signalling.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Ischemic Stroke and Traumatic Brain Injury: Epidemiology, Molecular Pathways, and Emerging Therapies.MedComm · 2026Review
- Nanoformulated fingolimod attenuates NLRP3 inflammasome activation and promotes functional recovery in a rat model of spinal cord injury.Spinal cord · 2026Article
- Pathological Roles of Astrocytes in Traumatic Brain Injury.CNS neuroscience & therapeutics · 2026Review
- Transcriptomic analysis of the physiological responses to injuries induced accompanying intracortical microelectrode implantation.Biomaterials · 2026Article
- Fingolimod as a Neuroprotective Agent in Ischemic Stroke: A Review of Preclinical and Clinical Evidence.Journal of clinical medicine · 2025Review
- Amorfrutin A ameliorates cerebral ischemia/reperfsion injuryThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Fingolimod Prevents Neuroinflammation but Has a Limited Effect on the Development of Ataxia in a Mouse Model for SCA1.International journal of molecular sciences · 2025Article
- Sphingosine-1-Phosphate Modulation in Neurological Disorders: Insights from MS and Stroke.Brain sciences · 2025Review
- Exosomes derived from bone marrow mesenchymal stem cells attenuate OGD/R-induced apoptosis in PC-12 cells via activation of the PI3K/AKT pathway.Journal of stem cells & regenerative medicine · 2025Article
- S1PR3 inhibition protects against LPS-induced ARDS by inhibiting NF-κB and improving mitochondrial oxidative phosphorylation.Journal of translational medicine · 2024Article
- S1PR3 suppresses the inflammatory response and extracellular matrix degradation in human nucleus pulposus cells.Experimental and therapeutic medicine · 2024Article
- Pharmacological Effects of FTY720 and its Derivatives.Current topics in medicinal chemistry · 2024Review
- Article
- [Knockout of S1PR3 attenuates acute lung injury in mice by inhibiting the MAPK pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Article
- Shared brain transcriptomic signature in TDP-43 type A FTLD patients with or without GRN mutations.Brain : a journal of neurology · 2022Article
- Molecular Pharmacology and Novel Potential Therapeutic Applications of Fingolimod.Frontiers in pharmacology · 2022Review
- Early-life fingolimod treatment improves intestinal homeostasis and pancreatic immune tolerance in non-obese diabetic mice.Acta pharmacologica Sinica · 2021Article
- Review
- Rationale for the use of sphingosine analogues in COVID-19 patients.Clinical medicine (London, England) · 2021Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fingolimod (FTY720) is used as an immunosuppressant for multiple sclerosis. Numerous studies indicated its neuroprotective effects in stroke. However, the mechanism remains to be elucidated. This study was intended to investigate the mechanisms of phosphorylated FTY720 (pFTY720), which was the principle active molecule in regulating astrocyte-mediated inflammatory responses induced by oxygen-glucose deprivation (OGD). Results demonstrated that pFTY720 could protect astrocytes against OGD-induced injury and inflammatory responses. It significantly decreased pro-inflammatory cytokines, including high mobility group box 1 (HMGB1) and tumour necrosis factor-α (TNF-α). Further, studies displayed that pFTY720 could prevent up-regulation of Toll-like receptor 2 (TLR2), phosphorylation of phosphoinositide 3-kinase (PI3K) and nuclear translocation of nuclear factor kappa B (NFκB) p65 subunit caused by OGD. Sphingosine-1-phosphate receptor 3 (S1PR3) knockdown could reverse the above change. Moreover, administration of TLR2/4 blocker abolished the protective effects of pFTY720. Taken together, this study reveals that pFTY720 depends on S1PR3 to protect astrocytes against OGD-induced neuroinflammation, due to inhibiting TLR2/4-PI3K-NFκB signalling pathway.
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Registered trials
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