Control of microglial neurotoxicity by the fractalkine receptor
| Autor: | Jar Chi Lee, Richard M. Ransohoff, Dan R. Littman, Donald N. Cook, Volodymyr Kostenko, Erik P. Pioro, Astrid E. Cardona, Ineke M. Dijkstra, Margaret E. Sasse, Ranjan Dutta, Steffen Jung, Stephen M. Dombrowski, Sergio A. Lira, De Ren Huang, Grahame J. Kidd, Sandra M. Cardona |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Central Nervous System
Lipopolysaccharides Green Fluorescent Proteins CX3C Chemokine Receptor 1 Mice Transgenic Nerve Tissue Proteins Mice CX3CR1 medicine Animals Motor Neuron Disease CX3CL1 Cells Cultured Neurons Analysis of Variance Microglia Cell Death business.industry General Neuroscience Neurodegeneration Calcium-Binding Proteins Microfilament Proteins Neurotoxicity Parkinson Disease medicine.disease Flow Cytometry Immunohistochemistry Oligodendrocyte Mice Inbred C57BL Disease Models Animal medicine.anatomical_structure Cytokines Neurotoxicity Syndromes Receptors Chemokine Neuron business Neuroscience Astrocyte |
| Zdroj: | Nature neuroscience. 9(7) |
| ISSN: | 1097-6256 |
| Popis: | Microglia, the resident inflammatory cells of the CNS, are the only CNS cells that express the fractalkine receptor (CX3CR1). Using three different in vivo models, we show that CX3CR1 deficiency dysregulates microglial responses, resulting in neurotoxicity. Following peripheral lipopolysaccharide injections, Cx3cr1−/− mice showed cell-autonomous microglial neurotoxicity. In a toxic model of Parkinson disease and a transgenic model of amyotrophic lateral sclerosis, Cx3cr1−/− mice showed more extensive neuronal cell loss than Cx3cr1+ littermate controls. Augmenting CX3CR1 signaling may protect against microglial neurotoxicity, whereas CNS penetration by pharmaceutical CX3CR1 antagonists could increase neuronal vulnerability. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|