Abstract
Our previous work has indicated that miR-155 expression induces inflammatory responses in ischemic cerebral tissues. However, the delicate regulation of miR-155-modifed inflammatory responses has remained enigmatic. In the present study, we found that autophagy is induced by ischemia through miR-155 and involved in neural injury. Subsequently, miR-155- induced autophagy modifies inflammatory responses through regulating TLR4/NF-κB pathway in ischemic cerebral tissues. Thus, miR-155 elevated autophagy is detrimental for ischemic cerebral injury and miR-155-induced autophagy modulates inflammatory responses through activating TLR4/NF-κB pathway.
Keywords:
autophagy; hypoxic damages; inflammatory response; ischemic cerebral tissues; ischemic stroke; miR-155..
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MeSH terms
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Administration, Oral
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Animals
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Autophagy / drug effects
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Autophagy / physiology*
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Cell Hypoxia / drug effects
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Cell Line, Transformed
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Chromones / administration & dosage
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Disease Models, Animal
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Enzyme Inhibitors / administration & dosage
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Gene Expression Regulation / drug effects
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Gene Expression Regulation / genetics*
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Glucose / deficiency
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Infarction, Middle Cerebral Artery / complications*
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Inflammation / etiology*
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Male
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic
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MicroRNAs / genetics
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MicroRNAs / metabolism*
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Morpholines / administration & dosage
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NF-kappa B / metabolism
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Neurologic Examination
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RNA, Messenger / metabolism
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Signal Transduction / drug effects
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Signal Transduction / genetics
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Toll-Like Receptor 4 / genetics
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Toll-Like Receptor 4 / metabolism
Substances
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Chromones
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Enzyme Inhibitors
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MicroRNAs
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Mirn155 microRNA, mouse
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Morpholines
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NF-kappa B
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RNA, Messenger
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Toll-Like Receptor 4
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2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
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Glucose