Methallothionein-3 contributes to vascular endothelial growth factor induction in a mouse model of choroidal neovascularization

Metallomics ◽  
2013 ◽  
Vol 5 (10) ◽  
pp. 1387 ◽  
Author(s):  
Jeong A Choi ◽  
Jong-uk Hwang ◽  
Young Hee Yoon ◽  
Jae-Young Koh
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Mouse Model ◽  
Choroidal Neovascularization ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals Human Vascular Endothelial Growth Factor A165 Expression Induces the Mouse Model of Neovascular Age-Related Macular Degeneration

Genes ◽  
2018 ◽  
Vol 9 (9) ◽  
pp. 438 ◽  
Author(s):  
Emmi Kokki ◽  
Tommi Karttunen ◽  
Venla Olsson ◽  
Kati Kinnunen ◽  
Seppo Ylä-Herttuala
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Gene Transfer ◽  
Mouse Model ◽  
Choroidal Neovascularization ◽  
Age Related Macular Degeneration ◽  
Vascular Endothelial ◽  
Time Points ◽  
Age Related ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) expression induces age-related macular degeneration (AMD), which is a common vision-threatening disease due to choroidal neovascularization and a fibrovascular membrane. We describe a mouse model of neovascular AMD with the local expression of human VEGF-A165 in the eye. We use a transgenic mouse in which human VEGF-A165 has been silenced with the loxP-STOP fragment. The choroidal neovascularization and human VEGF-A165 expression in the mouse are induced by subretinal adenoviral Cre gene delivery. Cre gene transfer is compared with adenoviral LacZ gene transfer control. We characterize the AMD phenotype and changes in the vasculature by using fluorescein angiography, optical coherence tomography, and immunohistochemistry. At early time points, mice exhibit increases in retinal thickness (348 ± 114 µm vs. 231 ± 32 µm) and choroidal neovascularization area (12000 ± 15174 µm2 vs. 2169 ± 3495 µm2) compared with the control. At later time points, choroidal neovascularization develops into subretinal fibrovascular membrane. Human VEGF-A165 expression lasts several weeks. In conclusion, the retinas display vascular abnormalities consistent with choroidal neovascularization. Together with immunohistochemical findings, these changes resemble clinical AMD-like ocular pathologies. We conclude that this mouse model of Cre-induced choroidal neovascularization is useful for mimicking the pathogenesis of AMD, studying the effects of human VEGF-A165 in the retina, and evaluating anti-VEGF treatments for choroidal neovascularization.

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