Age-related macular degeneration (AMD) in its Choroidal neovascularization (CNV) stage, where the growing neovessels invade the retina inducing photoreceptor degeneration, is the leading cause of vision loss among adults. Our lab has previously demonstrated that α2M and its receptor, LRP1, participate during retinal NV. Moreover, other authors propose LRP1 as a regulator of inflammatory responses. In the present study, we characterize the neovascular process and the pro-inflammatory profile, emphasizing on the level and localization of the α2M/LRP1 system in CNV. Experimentally, C57BL/6 adult mice were treated with four spots of argon green laser photocoagulation per eye. After 7 days of laser, the inflammatory and pro-angiogenic profile was analysed by qPCR assay while the protein levels of α2M and LRP1 were studied by WB. On choroid–RPE flatmounts stained with isolectin B4 (endotelial marker), the localization of mononuclear phagocyte cells and its levels of LRP1 were evaluated with F4/80 and Iba1 staining (macrophage and microglia) by IF by confocal microscopy. LRP1 levels on microglia were confirmed by Flow cytometry. We could observe on CNV animals high levels of both, pro-inflammatory and pro-angiogenic factors, as well as an elevated number of mononuclear phagocyte cells expressing LRP1 close to the CNV area. In this sense α2M and LRP1 showed change of expression, particularly on microglia cells. Further studies are needed to know the role of α2M/LRP1 on the CNV.