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Human Apolipoprotein(a) Kringle V Inhibits Ischemia-Induced Retinal Neovascularization via Suppression of Fibronectin-Mediated Angieogenesis

Cited 18 time in Web of Science Cited 20 time in Scopus
Authors

Lim, Yangmi; Jo, Dong Hyun; Kim, Jin Hyoung; Ahn, Jin-Hyung; Hwang, Yu Kyeong; Kang, Doug-Ku; Chang, Soo-Ik; Yu, Young Suk; Yoon, Yeup; Kim, Jeong Hun

Issue Date
2012-06
Publisher
American Diabetes Association
Citation
Diabetes, Vol.61 No.6, pp.1599-1608
Abstract
Retinal neovascularization is observed in progression of diabetic retinopathy. New vessels grow into the vitreous cavity in proliferative diabetic retinopathy, resulting in traction retinal detachment and vitreous hemorrhage. To overcome the catastrophic visual loss clue to these complications, efforts have been focused on the treatment of retinal neovascularization. In this study, we demonstrated the inhibitory effect of recombinant human apolipoprotein(a) kringle V (rhLK8) in an animal model of ischemia-induced retinal neovascularization. rhLK8 induced no definite toxicity on endothelial cells and retinal tissues at the therapeutic dosage. Interestingly, rhLK8 showed antiangiogenic effect, particularly on fibronectin-mediated migration of endothelial cells. Further experiments demonstrated high binding affinity of rhLK8 to alpha 3 beta 1 integrin, and suppression of it might be the mechanism of antiangiogenic effect of rhLK8. Furthermore, rhLK8 inhibited phosphorylation of focal adhesion kinase, resulting in suppression of activation of consequent p130CAS-Jun NH2-terminal kinase. Taken together, our data suggested the possible application of rhLK8 in the treatment of retinal neovascularization by suppression of fibronectin-mediated angiogenesis.
ISSN
0012-1797
URI
https://hdl.handle.net/10371/191637
DOI
https://doi.org/10.2337/db11-1541
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