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Ischemia-induced Neuronal Cell Death Is Mediated by Chemokine Receptor CX3CR1. | LitMetric

AI Article Synopsis

  • The chemokine fractalkine (CX3CL1) and its receptor CX3CR1 are important in understanding stroke's mechanisms, particularly how they interact in the central nervous system.
  • Recent research has found that CX3CR1 receptors are also present on hippocampal neurons, indicating they may influence both protective and harmful effects in brain cells.
  • Using a mouse model of stroke, it was shown that higher levels of CX3CR1 lead to increased neuronal death, while mice without CX3CR1 were more resistant to cell damage, suggesting targeting CX3CR1 could be a new treatment approach for stroke.

Article Abstract

The chemokine fractalkine (CX3CL1) and its receptor CX3CR1 play a fundamental role in the pathophysiology of stroke. Previous studies have focused on a paracrine interaction between neurons that produce fractalkine and microglia that express CX3CR1 receptors in the central nervous system. Recent findings have demonstrated the functional expression of CX3CR1 receptors by hippocampal neurons, suggesting their involvement in neuroprotective and neurodegenerative actions. To elucidate the roles of neuronal CX3CR1 in neurodegeneration induced by ischemic stroke, a mouse model of permanent middle cerebral artery occlusion (pMCAO) was employed. In the pMCAO mice, increased CX3CR1 levels, apoptosis-associated morphological changes, and Caspase 3-positive neuronal cells were observed in the striatum and in the hippocampus 24 hours after occlusion. Upregulation of CX3CR1 in ischemic neurons is associated with neuronal apoptotic cell death. In contrast, ischemia-induced apoptotic neuronal cell death was decreased in CX3CR1 deficient mice. Cultured primary hippocampal neurons obtained from CX3CR1 deficient mice were more resistant to glutamate-induced excitotoxicity by blocking calcium influx than those from wild-type mice. For the first time, we reported that neuronal CXCR1 mediates neuronal apoptotic cell death in ischemia. Our results suggest that modulating CXCR1 activity offers a novel therapeutic strategy for stroke.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5765008PMC
http://dx.doi.org/10.1038/s41598-017-18774-0DOI Listing

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