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

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 (H 2 O 2 ), while the knockdown of lncNALT rescued the viability, proliferation, migration, and invasion of RMECs treated with H 2 O 2 . 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. lncNALT interacts with HuR to increase the stability and expression levels of the PTEN lncNALT regulates HR via the PTEN/PI3K/AKT pathway lncNALT may be a potential diagnostic biomarker for HR