Adeno-Associated Virus-Mediated Expression of Vascular Endothelial Growth Factor Peptides Inhibits Retinal Neovascularization in a Mouse Model of Oxygen-Induced Retinopathy

2005 ◽  
Vol 16 (11) ◽  
pp. 1247-1254 ◽  
Author(s):  
Wen-Tao Deng ◽  
Zuan Yan ◽  
Astra Dinculescu ◽  
Jijing Pang ◽  
Jacqueline T. Teusner ◽  
...  
2021 ◽  
pp. 38-38
Author(s):  
Ning Yang ◽  
Xuejun He ◽  
Ningzhi Zhang ◽  
Yiqiao Xing

Inhibition of vascular endothelial growth factor (VEGF) has been widely applied in antineovascularization therapies. As a novel anti-VEGF agent, KH902 (conbercept) is designed to restrain pathological angiogenesis. However, the effects of KH902 on retinal hypoxia have not been well studied. In a mouse model of oxygen-induced retinopathy (OIR), we assessed retinal hypoxia at postnatal days 14 (P14) and P17, as well as retinal neovascularization (RNV) at P17. In addition, we evaluated the protein level of VEGF and galectin-1 (Gal-1). Changes of the neuroretinal structure were also examined. Our results indicated that KH902 could remit retinal hypoxia in OIR at P14 and P17, which was an exciting novel finding for KH902 function. Additionally, we confirmed that KH902 markedly reduces RNV. Our results indicated that administration of KH902 downregulated VEGF expression, as well as Gal-1. Damage of neuroretinal structure after KH902 injection was not observed, which was also an encouraging result. Our study suggests that KH902 plays a role in alleviating retinal hypoxia and that it could be used for the treatment of other neovascular ocular diseases.


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