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Luzhen Huang; EVA1A/TMEM166 regulates choroidal neovascularization by autophagy. Invest. Ophthalmol. Vis. Sci. 2018;59(9):362.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate the role of EVA1A/TMEM166 in choroidal neovascularization and the possible mechanisms.
Laser-induced CNV in EVA1A/TMEM166 transgenic and wild-type mice was used to study the effects of EVA1A/TMEM166 on angiogenesis in vivo. Fluorescein angiography was performed to evaluate the leakage area of each lesion. Plasmid-based gene transfer technology was used to increase EVA1A/TMEM166 expression and to study its effects on human umbilical vein endothelial cells (HUVECs) in vitro. Cell proliferation, migration, and tube formation were assessed. Quantitative real-time PCR and Western blot were used to measure expression of ATG7,VEGF,A2M,VTN and THBS1.
Laser treatment led to less CNV and vascular leakage in EVA1A/TMEM166 transgenic mice compared with wild-type mice. Upregulation of EVA1A/TMEM166, VEGF, VTN(Vitronectin), THBS1(thrombospondin-1),ATG7(autophagy-related protein 7) were detected in retina and choroidal tissue of laser- treated transgenic mice while A2M(Alpha-2-macroglobulin) expression was decreased . After transfection of HUVECs with a EVA1A/TMEM166 overexpression plasmid, cell proliferation, migration, and tube formation capacities were decreased.
EVA1A/TMEM166 overexpression reduced angiogenic effects in both a laser-induced CNV mouse model and HUVECs. EVA1A/TMEM166 may inhibit angiogenesis by up regulating autophagy and the expression of angiogenesis Inhibitors.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
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