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Lymphocytic Microparticles Modulate Angiogenic Properties of Macrophages in Laser-induced Choroidal
Houda Tahiri1,2, Samy Omri3, Chun Yang2
1Department of Pharmacology, Université de Montréal, Montréal, QC, Canada.
Abstract:
Pathological choroidal neovascularization (CNV) is the common cause of vision loss in patients with age-related macular degeneration (AMD). Macrophages possess potential angiogenic function in CNV. We have demonstrated that human T lymphocyte-derived microparticles (LMPs) exert a potent antiangiogenic effect in several pathological neovascularization models. In this study, we investigated the alteration of proangiogenic properties of macrophages by LMPs treatment in vitro and in vivo models. LMPs regulated the expression of several angiogenesis-related factors in macrophages and consequently stimulated their antiangiogenic effects evidenced by the suppression of the proliferation of human retinal endothelial cells in co-culture experiments. The involvement of CD36 receptor in LMPs uptake by macrophages was demonstrated by in vitro assays and by immunostaining of choroidal flat mounts. In addition, ex vivo experiments showed that CD36 mediates the antiangiogenic effect of LMPs in murine and human choroidal explants. Furthermore, intravitreal injection of LMPs in the mouse model of laser-induced CNV significantly suppressed CNV in CD36 dependent manner. The results of this study suggested an ability of LMPs to alter the gene expression pattern of angiogenesis-related factors in macrophages, which provide important information for a new therapeutic approach for efficiently interfering with both vascular and extravascular components of CNV.
Insights
Human T lymphocyte-derived microparticles (LMPs) reduce pathological choroidal neovascularization (CNV) by altering macrophage function. This discovery offers a novel therapeutic strategy for age-related macular degeneration (AMD).
Area of Science:
- Ophthalmology
- Immunology
- Angiogenesis Research
Background:
- Pathological choroidal neovascularization (CNV) is a primary cause of vision loss in age-related macular degeneration (AMD).
- Macrophages play a role in the angiogenic processes within CNV.
- Human T lymphocyte-derived microparticles (LMPs) have shown antiangiogenic effects in other models.
Purpose of the Study:
- To investigate how LMPs alter the proangiogenic properties of macrophages.
- To explore the therapeutic potential of LMPs in CNV models.
Main Methods:
- In vitro and in vivo studies using macrophages and CNV models.
- Assessing the effects of LMPs on angiogenesis-related factors and endothelial cell proliferation.
- Investigating the role of the CD36 receptor in LMP uptake and antiangiogenic effects.
- Laser-induced CNV mouse model and ex vivo choroidal explant experiments.
Main Results:
- LMPs modulated gene expression in macrophages, shifting them towards antiangiogenic functions.
- LMPs suppressed human retinal endothelial cell proliferation in co-culture.
- CD36 receptor was essential for LMP uptake and mediated their antiangiogenic effects in murine and human explants.
- Intravitreal LMPs significantly suppressed laser-induced CNV in mice in a CD36-dependent manner.
Conclusions:
- LMPs can reprogram macrophages to exert antiangiogenic effects, crucial for CNV.
- The CD36 receptor is key for mediating the therapeutic benefits of LMPs in CNV.
- LMPs represent a promising therapeutic strategy for targeting both vascular and extravascular components of CNV.
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