Effect of inhibitor of differentiation 1 deficiency on ocular neovascularization
10.3969/j.issn.1674-8115.2019.04.005
- Author:
Yi-Yun YAO
1
Author Information
1. Department of Ophthalmology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine
- Publication Type:Journal Article
- Keywords:
Hypoxia-inducible factor-1α (HIF-1α);
Inhibitor of differentiation-1 (ID1);
Ocular neovascularization;
Vascular endothelial growth factor receptor 1 (VEGFR1);
Vascular endothelial growth factor(VEGF)
- From:
Journal of Shanghai Jiaotong University(Medical Science)
2019;39(4):358-365
- CountryChina
- Language:Chinese
-
Abstract:
Objective • To study the effect of inhibitor of differentiation 1 (ID1) on ocular neovascularization. Methods • The oxygen-induced retinal neovascularization (OIR), laser-induced choroidal neovascularization (CNV) and over-expression of vascular endothelial growth factor (VEGF) (Rho-VEGF) transgenic mice were established. The localization and mRNA level of ID1 in retina of OIR mice and Rho-VEGF transgenic mice were determined by immunofluorescence staining and quantitative real-time PCR. Mice deficient in ID1 (ID1-/-) were used to induce retinal neovascularization in accordance with the above three models, and to compare the changes of ID1 on the number of retinal, subretinal and choroidal neovascularization areas. In order to explore the role ID1 in neovascularization, the numbers and areas of retinal, subretinal and choroidal neovascularization in the mice models with or without ID1 deficiency were compared. Its effect on the related factors, i.e. hypoxia-inducible factor-1α (HIF-1α), VEGF and vascular endothelial growth factor receptor 1/2 (VEGFR1/2) were also observed. Results • Mice deficient in ID1 showed a significant reduction in the area of neovascularization in these three models(P<0.05). Mice lacking ID1 showed reduced levels of HIF-1α, VEGF and VEGFR 1. Conclusion • ID1 promotes the expression of HIF-1α, VEGF and VEGFR1 in the retina and choroidal neovascularization during hypoxia and oxidative injury.
