Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8292322 | Biochemical and Biophysical Research Communications | 2018 | 7 Pages |
Abstract
choroidal neovascularization (CNV), a characteristic of wet age-related macular degeneration (AMD), causes severe vision loss among elderly patients. TANK-binding kinase 1 (TBK1) is a ubiquitously expressed serine-threonine kinase and is found to induce endothelial cells proliferation, represent a novel mediator of tumor angiogenesis and exert pro-inflammatory effect. However, the role of TBK1 in choroidal neovascularization has not been investigated so far. In this study, we found that the expression of TBK1 and VEGF was up-regulated in RF/6â¯A cells chemical hypoxia model and laser-induced mouse CNV model. Silencing of TBK1 suppressed the proliferation and tube formation activity of RF/6â¯A cells. Intravitreal injection of anti-TBK1 monoclonal antibody ameliorates CNV formation. Taken together, these findings exhibit a proangiogenic role for TBK1 via upregulating the expression of VEGF, and may suggest that TBK1 inhibition offers a unique and alternative method for prevention and treatment of AMD.
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Biochemistry
Authors
Kaixuan Cui, Shanshan Zhang, Xiaojuan Liu, Zhenzhen Yan, Lili Huang, Xiaowei Yang, Rongrong Zhu, Aimin Sang,