MicroRNA-155 Inhibits Polarization of Macrophages to M2-Type and Suppresses Choroidal Neovascularization

• DOI: 10.1007/s10753-017-0672-8
• Publication Date: 2017-09-30T05:17:34Z
• Authors: Pengfei Zhang; Hong Wang; Xueting Luo; Haiyun Liu; Bing Lu; Tong Li; Shiqi Yang; Qing Gu; Bin Li; Fenghua Wang; Xiaodong Sun
• Keywords: Male; Vascular Endothelial Growth Factor A; 0301 basic medicine; Laser Coagulation; Arginase; Neovascularization, Pathologic; Choroid; CCAAT-Enhancer-Binding Protein-beta; Macrophages; Transfection; Choroidal Neovascularization; Dinoprostone; beta-N-Acetylhexosaminidases; Mice, Inbred C57BL; Disease Models, Animal; MicroRNAs; 03 medical and health sciences; Phenotype; Lectins; Animals; Cells, Cultured

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.