Abstract
As the immune cells of the brain, microglia are crucial for the maintenance of brain function. The aims of the present study were to determine whether and how annexin-1 is able to affect microglial phenotype and migration in the lesion microenvironment. In the current experiment, we enhanced the interaction between annexin-1 and formyl peptide receptors in microglia and analyzed the function. We found that annexin-1 could polarize microglia to a beneficial phenotype and promote microglial migration to protect neurons from ischemia-like injury, and the annexin-1-mediated neuroprotective effect was dependent on the release of glutamate and ATP from the injured neurons.
Keywords:
Annexin-1; Microglia; Migration; Neuronal injury; Phenotype.
Copyright © 2014 Elsevier B.V. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenosine Triphosphate / pharmacology
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Animals
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Annexin A1 / genetics
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Annexin A1 / metabolism*
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Annexin A1 / pharmacology
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Calcium / metabolism
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Cell Movement / physiology
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Cell Survival / drug effects
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Cells, Cultured
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Cerebral Cortex / cytology
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Dose-Response Relationship, Drug
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Embryo, Mammalian
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Glucose / deficiency
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Glutamic Acid / pharmacology
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Hypoxia / prevention & control
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Mice
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Mice, Inbred BALB C
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Microglia / drug effects
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Microglia / metabolism*
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Neurons / drug effects
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Neurons / metabolism*
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Peptides / pharmacology
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Rats
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Rats, Sprague-Dawley
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Receptors, Formyl Peptide / genetics
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Receptors, Formyl Peptide / metabolism*
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Time Factors
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Up-Regulation / drug effects
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Up-Regulation / genetics
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Up-Regulation / physiology*
Substances
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Annexin A1
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Peptides
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Receptors, Formyl Peptide
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annexin A1 peptide (2-26)
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Glutamic Acid
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Adenosine Triphosphate
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Glucose
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Calcium