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Cerebrovascular inflammation and repair of the blood-brain barrier after stroke| old_uid | 11044 |
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| title | Cerebrovascular inflammation and repair of the blood-brain barrier after stroke |
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| start_date | 2016/02/29 |
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| schedule | 12h |
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| online | no |
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| location_info | Bât. IDEE, GHE entrée Est, Amphithéâtre Margaux Hemingway |
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| details | Cycle des conférences CRNL 2016 - Invité par Laurent BEZIN (TIGER) et Jean-François GHERSI-EGEA (FLUID) |
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| summary | Inflammation is a key host defence response that contributes to brain damage after ischemic injury, and is associated with poor outcome in stroke patients. Understanding the mechanisms of inflammation is critical for the development of new therapeutic approaches, and is a clinical priority. The inflammatory response after stroke occurs primarily at the blood-brain barrier (BBB), and cerebrovascular inflammation is driven by the cytokine interleukin-1 (IL-1), the action of which leads to a rapid degradation of the extracellular matrix (ECM) of the BBB, activation of endothelial cells and subsequent infiltration of circulating neurotoxic neutrophils into the brain. We have recently demonstrated that this mechanism of cerebrovascular inflammation occurs locally, but also in distant areas from the ischemic core leading to delayed neurodegeneration. We have found that ECM remodelling at the cerebrovasculature induces the generation of bioactive ECM fragments that are key regulators of IL-1-induced endothelial cell activation after cerebral ischaemia. ECM remodelling is regulated by the acute phase protein pentraxin-3 (PTX3), the expression of which is dependent on IL-1 in the injured brain, and we have found that PTX3 is a key mediator of brain repair mechanisms including astrogliosis, BBB repair, brain oedema resolution, angiogenesis and neurogenesis. This presentation will highlight these new mechanisms of neurotoxicity and brain tissue repair that could be targeted for the therapeutic treatment of ischemic stroke. |
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| responsibles | Béranger, Rossetti |
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