Suppression of choroidal neovascularization by silencing of long non-coding RNA IPW

Long noncoding RNAs (lncRNAs) have emerged as the key regulators in the pathogenesis of human disorders. This study aimed to investigate the role of lncRNA-IPW in the progression of choroidal neovascularization (CNV) and the underlying molecular mechanism. IPW was significantly up-regulated in the choroidal tissues of laser-induced CNV mice and in the endothelial cells in response to hypoxic stress. IPW silencing led to reduced formation of CNV in laser-induced CNV model and ex vivo choroidal sprouting model, which could achieve similar therapeutic effects of anti-VEGF on CNV formation. Silencing or transgenic overexpression of IPW could alter endothelial cell viability, proliferation, migration, and tube formation ability in vitro. Mechanistically, IPW silencing led to increased expression of miR-370. Increased miR-370 could mimic the effects of IPW silencing on CNV formation and endothelial angiogenic phenotypes in vivo and in vitro. This study suggests that IPW silencing is a promising strategy for the treatment of neovascular ocular diseases.

Automated summary

In this study, IPW was found to play a role in the progression of choroidal neovascularization (CNV) and could be a potential target for the treatment of neovascular ocular diseases. Silencing IPW led to reduced CNV formation and altered endothelial cell angiogenic phenotypes through upregulation of miR-370. These findings suggest that IPW silencing may be a promising therapeutic strategy for neovascular ocular diseases.