Abstract

VEGF-A and VEGF-B are proangiogenic and key regulating factors for blood vessel growth. This study aims to compare VEGF-A and VEGF-B levels in the serum and vitreous of patients with neovascular pathology versus non-neovascular pathology. Our findings showed vitreous VEGF-A and VEGF-B levels increased in patients with neovascular disease, with higher levels of VEGF-A compared to VEGF-B (p ≤ .05). In the diabetic retinopathy (DR) group, higher vitreous VEGF-A or VEGF-B were found in proliferative diabetic retinopathy (PDR) than in non-PDR. The strong correlation between VEGF-A and VEGF-B demonstrates a simultaneous pathological increase of cytokines (p < .001), suggesting besides VEGF-A, VEGF-B is another contributor to ocular pathologies involving angiogenesis. There was no correlation between vitreous and serum VEGF-A or VEGF-B; however, a correlation between vitreous (VEGF-A or VEGF-B) and macular volume (p < .05) in DR patients was found. Targeting VEGF-A and VEGF-B in macular and retinal vascular diseases, involving neovascularization, may improve treatment outcomes.

Highlights

  • Angiogenesis is one of the mechanisms responsible for neovascularization, in which new blood vessels are contrived from the preexisting ones (Roy et al, 2006)

  • We investigated two cytokines levels (VEGF-A and vascular endothelial growth factor (VEGF)-B) in vitreous and serum associated with neovascular eye pathologies: diabetic retinopathy (DR), age-related macular degeneration (AMD) and retinal vein occlusion (RVO)

  • Our results demonstrated that vitreous VEGF-A and VEGF-B are increased in patients with neovascular diseases as compared to the control group of patients with non-neovascular diseases

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Summary

Introduction

Angiogenesis is one of the mechanisms responsible for neovascularization, in which new blood vessels are contrived from the preexisting ones (Roy et al, 2006). Neovascularization is an essential physiological process like embryonic development and induces several pathological processes, for instance, tumour growth, rheumatoid arthritis, psoriasis, and ocular diseases such as age-related macular degeneration (AMD), retinal vein occlusion (RVO) and diabetic retinopathy (DR) (Ferrara et al, 2003). Alternative splicing results in several VEGF variants or isoforms (Penn et al, 2008). Carmeliet et al (1996) and Ferrara et al (1996) showed the essential role of VEGF-A in embryonic vasculogenesis and angiogenesis. VEGF-A induces an angiogenic response, essential in inflammation due to its capacity to increase vascular permeability and induce vascular leakage (Amadio et al, 2016). VEGFR-1 and VEGFR-2 regulate and signal physiological and pathological angiogenesis (Shibuya, 2006). Binding to VEGFR-1 promotes tumour growth, metastasis, and inflammation (Shibuya, 2006)

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