Stroke is a leading cause of long-term disability worldwide. Its highly complex pathogenesis is characterized by a deleterious cycle of deregulated processes at the neurovascular unit. Astrocytes that represent an important neurovascular unit component are critical to early protection of nervous tissue post-stroke. However, astrocyte activation (termed astrogliosis) in response to ischemia becomes increasingly dysregulated and maladaptive with time and majorly interferes with long-term functional recovery. Given this dualistic nature, a better understanding of molecular key players involved in astrocyte activation and their communication with other neurovascular unit cell types may aid in designing strategies for improved stroke recovery. In this regard, the bioactive phospholipid sphingosine-1-phosphate (S1P) provides an interesting target. Specifically, S1P receptors yielded first promising results. 

Repräsentativer Hirnschnitt, der die mRNA-Expression von Gfap (glial fibrillary acidic protein; violett) und S1pr3 (sphingosine-1-phosphate receptor 3; gelb) und deren Kolokalisation in der Glialnarbe drei Tage nach ischämischem Schlaganfall zeigt. Adapted from Matuskova et al. iScience 27, 110031 June 21, 2024. https://doi.org/10.1016/ j.isci.2024.110031

Related Funding

University of Augsburg „Forschungspotenziale besser nutzen!“ – funding period 2024 - 2026
 

Hjärnfonden: Cell-specific sphingosine-1-phoshate signaling alterations mediate neurovascular unit impairment in response to ischemia – funding period 2024 – 2025
 

Neurofonden: The role of S1P-S1pr3 signaling in ischemic stroke – funding period 2024
 

Crafoordska Stiftelse: The role of ischemia-induced S1P-S1pr3 signaling in astrocytes  – funding period 2022 – 2024
 

Sparbanken Stiftelse Färs & Frosta: Astrocytes in stroke – funding period 2019 – 2022

Related Publications

Matuskova Hana, Porschen Lisa T., Matthes Frank, Lindgren Arne G., Petzold Gabor C., Meissner Anja. Spatiotemporal sphingosine-1-phosphate receptor 3 expression within the cerebral vasculature after ischemic stroke. https://doi.org/10.1016/j.isci.2024.110031
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Matthes Frank, Matuskova Hana, Arkelius Kajsa, Ansar Saema, Lundgaard Iben, Meissner Anja. An improved method for physical separation of cerebral vasculature and parenchyma enables detection of blood-brain-barrier dysfunction. https://doi.org/10.3390/neurosci2010004
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Vanherle Lotte, Matuskova Hana, Don-Doncow Nicholas, Uhl Franziska E., Meissner Anja. Improving cerebrovascular function to increase neuronal recovery in neurodegeneration associated to cardiovascular disease. https://doi.org/10.3389/fcell.2020.00053
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Salas-Perdomo Angélica, Miró-Mur Francesc, Gallizioli Mattia, Brait Vanessa H., Justicia Carles, Meissner Anja, Urra Xabier, Chamorro Angel, Planas Anna M.. Role of the S1P pathway and inhibition by fingolimod in preventing hemorrhagic transformation after stroke. https://doi.org/10.1038/s41598-019-44845-5
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Yagi Kenji, Lidington Darcy, Wan Hoyee, Fares Jessica C., Meissner Anja, Sumiyoshi Manabu, Ai Jinglu, Foltz Warren D., Nedospasov Sergei A., Offermanns Stefan, Nagahiro Shinji, Macdonald R. Loch, Bolz Steffen-Sebastian. Therapeutically targeting tumor necrosis factor-α/Sphingosine-1-Phosphate signaling corrects myogenic reactivity in subarachnoid hemorrhage. https://doi.org/10.1161/strokeaha.114.006365
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