被撤回的出版物: LncRNA NEAT1 inhibition upregulates miR-16-5p to restrain the progression of sepsis-induced lung injury via suppressing BRD4 in a mouse model (Retracted article. See vol. 117, 2023)

Objective: Long non-coding RNAs (lncRNAs) are known to sponge microRNAs (miRNAs) to regulate biological processes. However, the role of nuclear paraspeckle assembly transcript 1 (NEAT1) binding miR-16-5p in sepsisinduced lung injury remains largely unknown. We aim to explore the effect of NEAT1 sponging miR-16-5p on sepsis-induced lung injury via regulating bromodomain containing 4 (BRD4). Methods: A mouse model of sepsis-induced lung injury was established. Expression of NEAT1, miR-16-5p and BRD4 was determined. The pulmonary edema, myeloperoxidase (MPO) activity, pathological changes, levels of inflammatory factors, cell viability and apoptosis in mouse lung tissues were evaluated. The binding relationships between NEAT1 and miR-16-5p, and between miR-16-5p and BRD4 were confirmed. Results: NEAT1 and BRD4 were upregulated while miR-16-5p was downregulated in sepsis-induced lung injury. NEAT1 inhibition or miR-16-5p elevation suppressed pulmonary edema, MPO activity, pathological changes, inflammation and apoptosis, and promoted cell viability in mouse lung tissues. NEAT1 bound with miR-16-5p and miR-16-5p targeted BRD4. Conclusion: NEAT1 inhibition upregulates miR-16-5p to repress the progression of sepsis-induced lung injury via downregulating BRD4.

Automated summary

NEAT1 inhibition upregulates miR-16-5p to repress the progression of sepsis-induced lung injury via downregulating BRD4. NEAT1 and BRD4 were upregulated while miR-16-5p was downregulated in sepsis-induced lung injury. Inhibition of NEAT1 or elevation of miR-16-5p suppressed pulmonary edema, MPO activity, pathological changes, inflammation and apoptosis, and promoted cell viability in mouse lung tissues.