Abstract
Traumatic brain injury promotes rapid induction of microglial cells and infiltration of peripheral macrophages to the injury sites. Such inflammatory responses are mediated by the activation and migration of immune cells, which are influenced by the actin cytoskeleton remodeling. In this study, we observed that the phosphorylation and expressions of ezrin-radixin-moesin (ERM) proteins, which are linkers for cell surface with actin cytoskeleton, are induced in the activated microglia/macrophages, whereas ERM molecules are only marginally expressed in quiescent microglia in the normal brain. These results suggest that ERM activation in the injury penumbra is implicated in the inflammatory immune responses after traumatic brain injury.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Brain Injuries / etiology
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Brain Injuries / metabolism*
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Brain Injuries / pathology
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Cerebral Cortex / metabolism*
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Cerebral Cortex / pathology
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Cold Temperature / adverse effects*
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Cytoskeletal Proteins / biosynthesis*
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Cytoskeletal Proteins / genetics
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Disease Models, Animal
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Gliosis / etiology
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Gliosis / metabolism
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Gliosis / pathology
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Macrophage Activation / genetics
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Male
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Membrane Proteins / biosynthesis*
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Membrane Proteins / genetics
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Mice
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Mice, Inbred C57BL
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Microfilament Proteins / genetics
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Microfilament Proteins / metabolism
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Microglia / metabolism*
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Microglia / pathology
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Resting Phase, Cell Cycle / genetics
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Time Factors
Substances
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Cytoskeletal Proteins
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Membrane Proteins
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Microfilament Proteins
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ezrin
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moesin
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radixin