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• W2783048831 abstract "Analysis of microRNA (miR) expression in the central nervous system white matter of SJL mice infected with the BeAn strain of Theiler’s murine encephalomyelitis virus (TMEV) revealed a significant reduction of miR-219, a critical regulator of myelin assembly and repair. Restoration of miR-219 expression by intranasal administration of a synthetic miR-219 mimic before disease onset ameliorates clinical disease, reduces neurogliosis, and partially recovers motor and sensorimotor function by negatively regulating proinflammatory cytokines and virus RNA replication. Moreover, RNA sequencing of host lesions showed that miR-219 significantly downregulated two genes essential for the biosynthetic cholesterol pathway, Cyp51 (lanosterol 14-α-demethylase) and Srebf1 (sterol regulatory element-binding protein-1), and reduced cholesterol biosynthesis in infected mice and rat CG-4 glial precursor cells in culture. The change in cholesterol biosynthesis had both anti-inflammatory and anti-viral effects. Because RNA viruses hijack endoplasmic reticulum double-layered membranes to provide a platform for RNA virus replication and are dependent on endogenous pools of cholesterol, miR-219 interference with cholesterol biosynthesis interfered virus RNA replication. These findings demonstrate that miR-219 inhibits TMEV-induced demyelinating disease through its anti-inflammatory and anti-viral properties. Analysis of microRNA (miR) expression in the central nervous system white matter of SJL mice infected with the BeAn strain of Theiler’s murine encephalomyelitis virus (TMEV) revealed a significant reduction of miR-219, a critical regulator of myelin assembly and repair. Restoration of miR-219 expression by intranasal administration of a synthetic miR-219 mimic before disease onset ameliorates clinical disease, reduces neurogliosis, and partially recovers motor and sensorimotor function by negatively regulating proinflammatory cytokines and virus RNA replication. Moreover, RNA sequencing of host lesions showed that miR-219 significantly downregulated two genes essential for the biosynthetic cholesterol pathway, Cyp51 (lanosterol 14-α-demethylase) and Srebf1 (sterol regulatory element-binding protein-1), and reduced cholesterol biosynthesis in infected mice and rat CG-4 glial precursor cells in culture. The change in cholesterol biosynthesis had both anti-inflammatory and anti-viral effects. Because RNA viruses hijack endoplasmic reticulum double-layered membranes to provide a platform for RNA virus replication and are dependent on endogenous pools of cholesterol, miR-219 interference with cholesterol biosynthesis interfered virus RNA replication. These findings demonstrate that miR-219 inhibits TMEV-induced demyelinating disease through its anti-inflammatory and anti-viral properties." @default.
• W2783048831 created "2018-01-26" @default.
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• W2783048831 date "2018-03-01" @default.
• W2783048831 modified "2023-10-16" @default.
• W2783048831 title "microRNA-219 Reduces Viral Load and Pathologic Changes in Theiler's Virus-Induced Demyelinating Disease" @default.
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• W2783048831 cites W1988500121 @default.
• W2783048831 cites W1991439411 @default.
• W2783048831 cites W1997199017 @default.
• W2783048831 cites W2012620164 @default.
• W2783048831 cites W2016453349 @default.
• W2783048831 cites W2024556668 @default.
• W2783048831 cites W2028617079 @default.
• W2783048831 cites W2032102818 @default.
• W2783048831 cites W2033815392 @default.
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• W2783048831 cites W2035461575 @default.
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• W2783048831 cites W2037897155 @default.
• W2783048831 cites W2039551908 @default.
• W2783048831 cites W2049868800 @default.
• W2783048831 cites W2059994807 @default.
• W2783048831 cites W2063653640 @default.
• W2783048831 cites W2066124024 @default.
• W2783048831 cites W2071638524 @default.
• W2783048831 cites W2077019993 @default.
• W2783048831 cites W2077971415 @default.
• W2783048831 cites W2079557335 @default.
• W2783048831 cites W2084435762 @default.
• W2783048831 cites W2084566588 @default.
• W2783048831 cites W2086847869 @default.
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• W2783048831 cites W2102562492 @default.
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• W2783048831 cites W2130116522 @default.
• W2783048831 cites W2132730003 @default.
• W2783048831 cites W2134587746 @default.
• W2783048831 cites W2134629862 @default.
• W2783048831 cites W2138207763 @default.
• W2783048831 cites W2143890525 @default.
• W2783048831 cites W2150316403 @default.
• W2783048831 cites W2162674813 @default.
• W2783048831 cites W2166915947 @default.
• W2783048831 cites W2191790139 @default.
• W2783048831 cites W2209395704 @default.
• W2783048831 cites W2293644396 @default.
• W2783048831 cites W2309638858 @default.
• W2783048831 cites W2325222489 @default.
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• W2783048831 doi "https://doi.org/10.1016/j.ymthe.2018.01.008" @default.
• W2783048831 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5910888" @default.
• W2783048831 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29433936" @default.
• W2783048831 hasPublicationYear "2018" @default.
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