To explore the correlation between the level of Angiotensin II (Ang II) and corneal angiogenesis, the rat model of CRNV was established using alkali-burn, while the human umbilical vein endothelial cells (HUVECs) were stimulated using VEGF to induce the CRNV cells in vitro.
The purpose of the study is to evaluate the usefulness of OCTA to monitor regression of corneal vessels following anti-VEGF (vascular endothelial growth factor) treatment using a previously established corneal vascularisation rabbit model.
MMP14-containing exosomes may be involved in the regulation of corneal neovascularization through degradation of VEGFR1 and VEGFA-induced endothelial cell proliferation and migration.
The aim of the present study was to evaluate the ability of HGF and KGF to influence VEGF and its receptor, kinase insert domain receptor (Flk‑1) in corneal injury and CNV in rats induced by ultraviolet radiation (UVR).
Tear film levels of interleukin- (IL-) 6, IL-8, and vascular endothelial growth factor (VEGF) were investigated over time, and preoperative concentrations were linked to corneal neovascularization and pterygium size.
The results from <i>in vivo</i> tests such as ocular vessels observation, hematoxylin & eosin (H&E) stain, and metalloproteinases (MMP)/vascular endothelial growth factor (VEGF) quantification revealed the mice's eyes with corneal NV treated by eye drops containing GNP-KA once daily for 7 days had better therapeutic effects with less vessels in-growths in the cornea, compared to the KA solution group by reducing the production of MMP and VEGF in the cornea.
The long-term effect of tacrolimus on alkali burn-induced corneal neovascularization and inflammation surpasses that of anti-vascular endothelial growth factor.
Topical administration of the three axitinib concentrations inhibited CNV in rabbits, blocking both vascular endothelial growth factor and platelet-derived growth factor pathways.
These include inhibitory effects on proinflammatory mediators, such as IL-1β, IL-6, IL-12, CXCL1, MCP-1, MIP-2, vascular endothelial growth factor (VEGF)-A, matrix metalloproteinase 9 (MMP-9), and proinflammatory miRNA, such as miR-155, miR-132, and miR-223, which are involved in SK pathogenesis and corneal neovascularization.
Histopathological analysis and the expression level of the pro-angiogenic genes vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP9) revealed that chronic nicotine administration enhanced alkali burn-induced corneal neovascularization.
Down-regulation of miR-184 is associated with up-regulation of VEGF and Wnt/β-catenin expression as well as corneal neovascularization, indicating that miR-184 negatively regulates corneal neovascularization.
Subconjunctival bevacizumab helps to regress CNV due to a decrease in corneal VEGF levels and might prove beneficial for use in clinical conditions leading to CNV.
In a rat corneal vascularization model, DT18 demonstrated significant and specific antiangiogenic activity, as evidenced by the reduced area and vessel number in VEGF-induced corneal angiogenesis.
Herpes simplex virus (HSV) causes a chronic immuno-inflammatory response in the eye that may result in corneal neovascularization during blinding immunopathological lesion stromal keratitis (SK). miR-132 is a highly conserved miRNA that is induced in endothelial cells in response to growth factors, such as vascular endothelial growth factor (VEGF).