LncNALT knockdown ameliorates hypertensive retinopathy via PTEN/PI3K/AKT pathway

Abstract

ABSTRACT This study aimed to explore the role of the long non-coding RNA NOTCH1-associated lncRNA in T cell acute lymphoblastic leukemia (lncNALT) in the pathogenesis of hypertensive retinopathy (HR). LncNALT expression levels were determined using reverse transcription-quantitative polymerase chain reaction. The effects of lncNALT knockdown on the viability, proliferation, migration, and invasion of human retinal microvascular endothelial cells (RMECs) were determined via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide, 5-ethynyl-2’-deoxyuridine staining, and Transwell assays. Protein expression levels were determined using western blotting. We found that lncNALT expression levels were increased in RMECs treated with hydrogen peroxide (H2O2), while the knockdown of lncNALT rescued the viability, proliferation, migration, and invasion of RMECs treated with H2O2. Moreover, lncNALT interacted with ELAV like RNA binding protein 1 to affect the phosphatase and tensin homolog (PTEN) expression. Knockdown of lncNALT enhanced the viability, proliferation, migration, and invasion of RMECs via the PTEN/phosphoinositide 3-kinase (PI3K)/serine-threonine kinase (AKT) pathway. Taken together, knockdown of lncNALT enhanced the viability, proliferation, migration, and invasion of RMECs via the PTEN/PI3K/AKT pathway, suggesting that lncNALT could be a potential therapeutic target for patients with HR.