STUDY OF LRP1 IN CELLULAR INFLAMMATORY COMPONENT DURING CHOROIDAL NEOVASCULARIZATION

TOVO, A; SUBIRADA PV; VAGLIENTI MV; LUNA JD; SANCHEZ, MC; CHIABRANDO, GA; BARCELONA PF

Mar del Plata

Congreso; SAIC 2022 (XLVII Reunión Anual de Sociedad Argentina en Investigación Clínica); 2022

Sociedad Argentina en Investigación Clínica

Age-related macular degeneration (AMD) in its Choroidal Neovascularization (CNV) stage is the leading cause of vision loss among adults. Mononuclear phagocytic cells (MPCs), such as resident microglia and monocyte-derived macrophages, collaborate in establish a chronic inflammatory state that can lead to the onset of CNV. The multi-ligand, Low density lipoprotein receptor-related protein 1 (LRP1) is a ligand-dependent anti-inflammatory factor expressed in the cell inflammatory component, including macrophages and microglia. However, the role of LRP1 in CNV is not established yet. In the present study we aim to characterize the LRP1 levels and localization during CNV progression in a mouse model of CNV induce by laser. C57BL/6 adult mice were treated with four spots of argon green laser photocoagulation per eye. At 1, 4, 7, 14 and 21 days after laser, mice were sacrificed and choroid tissue was processed by Western Blot to study LRP1 protein levels. At 4 days after laser, TNFα and LRP1 transcript levels were analyzed by qRT PCR. The LRP1 expression in peripheral blood monocytes and MPCs from choroids tissue were evaluated by FACS assays.We could observe on choroids tissue from CNV animals increased levels of LRP1 at 1 and 4 days after laser. At 4 days after laser, the mRNA levels of pro-inflammatory cytokine, TNFα increased. In addition, the number of peripheral blood monocytes and their LRP1 expression were increases on CNV mice respect to control animals. However, LRP1 mRNA levels was unmodified on choroid. In conclusion, we observed increased LRP1 levels in early stages of CNV progression associated with enhanced pro inflammatory cytokine expressions, which was reverted after 4 days. These results suggest that the increased levels of LRP1 in CNV is due to MPC infiltration from circulating monocytes and resident microglial cells. Further studies are needed to determinate the role of LRP1 on these cells during CNV.