Abstract
BackgroundHypoxia and nitric oxide (NO) play important roles in the onset and progression of glaucoma. Vascular endothelial growth factor (VEGF) is one of the main factors responsive to hypoxia and NO. In this study, we investigated the association between the BstUI C/T VEGF gene polymorphism and primary open angle glaucoma (POAG).Methods60 POAG patients and 78 healthy volunteers were enrolled in this study. The most frequently observed polymorphism in the VEGF gene is BstUI C/T, which was located 460 nucleotides upstream of the gene. The polymorphism was observed using polymerase chain reaction-based restriction analysis.ResultsSignificant differences were observed in the distribution of the polymorphism between control subjects and POAG patients (p = 0.003). C/C homozygotes are absent in the control group; therefore, this genotype represents a suitable genetic maker for POAG.ConclusionsHypoxia and NO may be involved in the pathway whereby the VEGF-460 polymorphism regulates POAG. Furthermore, homozygous C/C VEGF genotype is a useful maker for Chinese POAG.BackgroundHypoxia and nitric oxide (NO) play important roles in the onset and progression of glaucoma. Vascular endothelial growth factor (VEGF) is one of the main factors responsive to hypoxia and NO. In this study, we investigated the association between the BstUI C/T VEGF gene polymorphism and primary open angle glaucoma (POAG).Methods60 POAG patients and 78 healthy volunteers were enrolled in this study. The most frequently observed polymorphism in the VEGF gene is BstUI C/T, which was located 460 nucleotides upstream of the gene. The polymorphism was observed using polymerase chain reaction-based restriction analysis.ResultsSignificant differences were observed in the distribution of the polymorphism between control subjects and POAG patients (p = 0.003). C/C homozygotes are absent in the control group; therefore, this genotype represents a suitable genetic maker for POAGConclusionsHypoxia and NO may be involved in the pathway whereby the VEGF-460 polymorphism regulates POAG. Furthermore, homozygous C/C VEGF genotype is a useful maker for Chinese POAG.
Highlights
Various circulatory abnormalities have been cited as involved in etiology of glaucomatous optic neuropathy.[1,2] Prominent in the disease is vascular regulatory factor itself.[3]
Vascular endothelial growth factor (VEGF)-induced angiogenesis might not be the primary factor in this relationship
VEGF is a cytokine, and our laboratory has demonstrated primary open angle glaucoma (POAG)’s positive association with many cytokines: e.g., tumor necrosis factor alpha[18] and interleukin-1.19 Pharmacological neuroprotection via inhibition of nitric oxide (NO) and hypoxia may prove useful in treating glaucoma.[5,6]
Summary
Various circulatory abnormalities have been cited as involved in etiology of glaucomatous optic neuropathy.[1,2] Prominent in the disease is vascular regulatory factor itself.[3]. Kotiloski H et al observed that NO concentrations in aqueous humour were slightly higher in glaucoma patients than in controls.[4] Galassi F et al suggested disorders of NO regulatory processes as be involved in modulating blood supply to the optic nerve and in aqueous humour outflow.[1] Becquet et al suggested NO acting at the level of ciliary muscle as well as on aqueous outflow pathway (trabecular meshwork, Schlemms’ canal, and collecting channels), influencing ocular hydrodynamics.[6] It is known that topical or intracameral application of NO donors alter aqueous humour outflow.[7] Neufeld AH et al proved induction of nitric-oxide synthesis (NOS-2) in an optic nerve head moderately raising IOP level. Background: Hypoxia and nitric oxide (NO) play important roles in the onset and progression of glaucoma. Homozygous C/C VEGF genotype is a useful maker for Chinese POAG
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