Long-chain non-coding RNA MALAT1 upregulates the MMP-2 signaling pathway by inhibiting miR-106a-5p in murine oxygen- induced retinopathy

Abstract

Retinopathy of prematurity (ROP) is a blinding eye disease in children that is characterized by the formation of neovascularization in the retina; current treatments for this disease risk retinal damage and visual impairment. This study aimed to investigate the relationship between metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), miR-106a-5p, and matrix metalloproteinase 2 (MMP-2) in an oxygen-induced retinopathy mouse model and hypoxia-induced human retinal endothelial cells and to elucidate whether MALAT1 upregulates MMP-2 signaling by inhibiting miR-106a-5p. The role of this pathway in oxygen-induced murine retinopathy and its underlying mechanism were also investigated. MALAT1 inhibited the expression of miR-106a-5p and enhanced the expression of MMP-2, which in turn caused a series of pathological changes, such as the formation of new blood vessels in the retina. In addition, knockdown of MALAT1 can downregulate the expression of MMP-2 by sponging miR-106a-5p and inhibiting cell proliferation, migration, and tube-forming ability. In conclusion, our findings suggest that MALAT1 may contribute to the occurrence and development of ROP by inhibiting miR-106a-5p and increasing the expression of MMP-2, thus providing a new perspective for the targeted therapy of ROP.