Effects of Dual Inhibition of VEGF-A and Angpt-2 on Angiogenesis and Lymphangiogenesis in an Alkali-Induced Corneal Injury Model
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View abstract on PubMed
Summary
This summary is machine-generated.Dual inhibition of VEGFA and ANGPT2 effectively reduces corneal neovascularization (CNV) after alkali injury. This targeted therapy shows promise for treating CNV by inhibiting blood vessel growth without affecting corneal thickness.
Area Of Science
- Ophthalmology
- Vascular Biology
- Immunology
Background
- Corneal neovascularization (CNV) impairs vision after injury and transplantation.
- CNV is often associated with lymphangiogenesis and inflammation.
- Alkali injury is a common cause and model for CNV.
Purpose Of The Study
- To evaluate the therapeutic potential of anti-VEGFA, anti-ANGPT2, and a bispecific antibody (BsAb) against VEGFA and ANGPT2 in a mouse model of corneal alkali injury.
- To investigate the effects of these treatments on angiogenesis, lymphangiogenesis, and related gene expression.
Main Methods
- Corneal alkali injury model in mice.
- Subconjunctival injection of anti-VEGFA antibody, anti-ANGPT2 antibody, or BsAb.
- Assessment of CNV using anterior segment optical coherence tomography (OCT) and whole-mount immunostaining.
- Gene expression analysis using RT-qPCR.
Main Results
- Anti-VEGFA_ab, anti-ANGPT2_ab, and BsAb treatments inhibited angiogenesis but not lymphangiogenesis or corneal thickness.
- Alkali injury increased mRNA levels of Vegfa, Angpt2, Il1b, and Cx3cr1.
- BsAb suppressed Vegfa and Cx3cr1 induction and enhanced Angpt1 mRNA levels.
Conclusions
- Dual inhibition of VEGFA and ANGPT2 is a promising therapeutic strategy for corneal neovascularization.
- Targeting both pathways offers a potential treatment for vision impairment caused by CNV.
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