Conditional knockdown of tubedown-1 in endothelial cells leads to neovascular retinopathy.

摘要: Purpose Identification of novel proteins involved in retinal neovascularization may facilitate new and more effective molecular-based treatments for proliferative retinopathy. Tubedown-1 (Tbdn-1) is a protein that shows homology to the yeast acetyltransferase subunit NAT1 copurifies with an activity. Tbdn-1 expressed normal endothelium but specifically suppressed endothelial cells from patients diabetic The purpose this study was investigate importance expression blood vessels vivo. Methods A bitransgenic mouse model enables conditional knockdown produced studied using molecular, histologic, immunohistochemical techniques morphometric analysis. Results Tbdn-1-suppressed mice exhibited choroidal intra- preretinal fibrovascular lesions similar human retinopathies. Retinal observed increased severity prolonged suppression Tbdn-1. In comparison retina, displayed alterations basement membrane distribution glial myofibroblastic cells. Moreover, pathologic consequences were restricted retina choroid. Conclusions These results indicate maintenance important vessel homeostasis controlling adults. Restoration and/or activity provide approach treating