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Galectin-1 expression imprints a neurovascular phenotype in proliferative retinopathies and delineates responses to
Magali E Ridano1, Paula V Subirada1, María C Paz1
1Centro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina.
Abstract:
Neovascular retinopathies are leading causes of irreversible blindness. Although vascular endothelial growth factor (VEGF) inhibitors have been established as the mainstay of current treatment, clinical management of these diseases is still limited. As retinal impairment involves abnormal neovascularization and neuronal degeneration, we evaluated here the involvement of galectin-1 in vascular and non-vascular alterations associated with retinopathies, using the oxygen-induced retinopathy (OIR) model. Postnatal day 17 OIR mouse retinas showed the highest neovascular profile and exhibited neuro-glial injury as well as retinal functional loss, which persisted until P26 OIR. Concomitant to VEGF up-regulation, galectin-1 was highly expressed in P17 OIR retinas and it was mainly localized in neovascular tufts. In addition, OIR induced remodelling of cell surface glycophenotype leading to exposure of galectin-1-specific glycan epitopes. Whereas VEGF returned to baseline levels at P26, increased galectin-1 expression persisted until this time period. Remarkably, although anti-VEGF treatment in P17 OIR improved retinal vascularization, neither galectin-1 expression nor non-vascular and functional alterations were attenuated. However, this functional defect was partially prevented in galectin-1-deficient (Lgals1-/-) OIR mice, suggesting the importance of targeting both VEGF and galectin-1 as non-redundant independent pathways. Supporting the clinical relevance of these findings, we found increased levels of galectin-1 in aqueous humor from patients with proliferative diabetic retinopathy and neovascular glaucoma. Thus, using an OIR model and human samples, we identified a role for galectin-1 accompanying vascular and non-vascular retinal alterations in neovascular retinopathies.
Insights
Galectin-1 plays a key role in neovascular retinopathies, contributing to vision loss beyond vascular endothelial growth factor (VEGF) effects. Targeting both galectin-1 and VEGF may improve treatment for these blinding conditions.
Area of Science:
- Ophthalmology
- Molecular Biology
- Immunology
Background:
- Neovascular retinopathies cause irreversible blindness, with current treatments like VEGF inhibitors having limitations.
- Retinal damage in these conditions involves abnormal blood vessel growth and nerve cell degeneration.
Purpose of the Study:
- To investigate the role of galectin-1 in vascular and non-vascular changes in oxygen-induced retinopathy (OIR), a model for neovascular retinopathies.
- To assess the therapeutic potential of targeting galectin-1 alongside VEGF.
Main Methods:
- Utilized the oxygen-induced retinopathy (OIR) mouse model to study retinal changes.
- Analyzed galectin-1 and VEGF expression, glycophenotype remodeling, and neuro-glial injury.
- Assessed the effects of anti-VEGF treatment and galectin-1 deficiency (Lgals1-/-) on retinal function and vascularization.
- Measured galectin-1 levels in aqueous humor from patients with proliferative diabetic retinopathy and neovascular glaucoma.
Main Results:
- OIR retinas showed significant neovascularization, neuro-glial injury, and functional loss, with high expression of galectin-1 localized in neovascular tufts.
- While anti-VEGF treatment improved vascularization, it did not affect galectin-1 expression or functional deficits.
- Galectin-1-deficient mice showed partial prevention of functional defects, indicating its independent role.
- Elevated galectin-1 levels were found in human patients with proliferative diabetic retinopathy and neovascular glaucoma.
Conclusions:
- Galectin-1 is involved in both vascular and non-vascular retinal alterations in neovascular retinopathies.
- Targeting both VEGF and galectin-1 represents a promising, non-redundant therapeutic strategy for these blinding diseases.
- Galectin-1's presence in patient samples supports its clinical relevance in neovascular retinopathies.
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