Abstract
Purpose :
M2-type macrophages play great role in the development of choroidal neovascularization (CNV). Thus, inhibition of M2 macrophage polarization may provide an alternative to anti-VEGF therapy. This study evaluated the role of C/EBPβ in M2 macrophage polarization. We also assessed whether microRNA-155 could inhibit polarization of macrophages to M2-type via targeting C/EBPβ and suppress CNV formation in laser-induced mice CNV model.
Methods :
M2 macrophage polarization and the expression of C/EBPβ were examined by Western blotting, real time PCR and immunohistochemistry on day 1,3,7 after laser-induced CNV formation in C57BL/6J mice.The effect of microRNA-155 on M2 macrophage polarization was evaluated in the CNV model by Western blotting, real time PCR and immunohistochemistry at the same time points after intravitreal injection of microRNA-155 mimics. To evaluate the role of microRNA-155 on CNV development, eyes of mice CNV model were examined by fluorescein angiography, choroidal flatmounts on day 7 after intravitreal injection.
Results :
Arg-1+Ym-1+M2 macrophage and the expression of C/EBPβ were significantly up-regulated in mice CNV model, while microRNA-155 could inhibit Arg-1+Ym-1+M2 macrophage polarization via targeting C/EBPβ in mice CNV model. Intravitreal injection of microRNA-155 mimics inhibited CNV leakage and neovascularization.
Conclusions :
MicroRNA-155 modulating C/EBPβ plays great role in M2 macrophage polarizaiton, while microRNA-155 mimics could suppress CNV by inhibiting M2 macrophages polarization.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.