Abstract
Arg-1+Ym-1+ M2-type macrophages play essential roles in the development of choroidal neovascularization (CNV). Thus, inhibition of M2-type macrophages may be effective in suppressing CNV. However, the potential mechanisms of macrophage polarization during development of CNV remain unclear. In this study, we report that microRNA-155 (miR-155) inhibited M2 polarization by targeting C/EBPβ in CNV model mice and in bone marrow-derived primary macrophages. Moreover, our data show that intravitreous injection of miR-155 mimics suppressed subretinal leakage and neovascularization. Therefore, we conclude that C/EBPβ plays a significant role in M2 macrophage polarization in CNV model, while miR-155 mimics could suppress CNV by inhibiting C/EBPβ activity and M2 macrophage polarization.
Keywords:
C/EBPβ; choroidal neovascularization; macrophages; miRNA-155; polarization.
MeSH terms
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Animals
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Arginase / genetics
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Arginase / metabolism
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CCAAT-Enhancer-Binding Protein-beta / genetics
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CCAAT-Enhancer-Binding Protein-beta / metabolism
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Cells, Cultured
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Choroid / metabolism*
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Choroid / pathology
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Choroidal Neovascularization / genetics
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Choroidal Neovascularization / metabolism
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Choroidal Neovascularization / pathology
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Choroidal Neovascularization / prevention & control*
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Dinoprostone / pharmacology
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Disease Models, Animal
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Laser Coagulation
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Lectins / genetics
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Lectins / metabolism
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Macrophages / drug effects
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Macrophages / metabolism*
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Macrophages / pathology
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Male
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Mice, Inbred C57BL
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MicroRNAs / genetics
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MicroRNAs / metabolism*
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Neovascularization, Pathologic*
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Phenotype
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Transfection
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Vascular Endothelial Growth Factor A / metabolism
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beta-N-Acetylhexosaminidases / genetics
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beta-N-Acetylhexosaminidases / metabolism
Substances
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CCAAT-Enhancer-Binding Protein-beta
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Cebpb protein, mouse
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Lectins
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MicroRNAs
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Mirn155 microRNA, mouse
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Vascular Endothelial Growth Factor A
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vascular endothelial growth factor A, mouse
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Chil3 protein, mouse
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beta-N-Acetylhexosaminidases
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Arg1 protein, mouse
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Arginase
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Dinoprostone