Knockdown of lncRNA-ASLNC12002 alleviates epithelial-mesenchymal transition of type II alveolar epithelial cells in sepsis-induced acute respiratory distress syndrome

Patients with sepsis-induced acute respiratory distress syndrome (ARDS) have higher mortality and poor prognosis than pneumonia-induced ARDS. Pulmonary fibrosis is an irreversible accumulation of connective tissue in the interstitium of the lung and closely associated with the epithelial-mesenchymal transition (EMT) of type II alveolar epithelial cells (AECIIs). Therefore, it is undoubtedly worth studying whether the EMT of AECIIs in sepsis-induced ARDS patients is different from that in patients with pneumonia-induced ARDS in the regulatory mechanism. Here, we will report for the first time that an lncRNA-ASLNC12002 is highly expressed in AECIIs of patients with sepsis-induced pneumonia and promotes EMT in AECIIs. The research results showed that the expression of ASLNC12002 in AECIIs derived from patients with sepsis-induced ARDS is significantly higher than that in normal people and pneumonia-induced ARDS patients. Mechanism research showed that ASLNC12002 can cause the inactivation of the anti-EMT pathway NR2F2/miR128-3p/Snail1 by acting as the sponge of miR128-3p. Functional experiments showed that targeted silencing of ASLNC12002 could effectively inhibit EMT progression in AECIIs of patients with sepsis-induced pneumonia by restoring NR2F2/miR128-3p/Snail1 pathway. In a word, our study shows for the first time that the inactivation of NR2F2/miR128-3p/Snail1 pathway caused by the enhanced expression of ASLNC12002 is the direct reason why AECIIs in sepsis-induced ARDS patients are prone to get EMT progress. ASLNC12002 has the potential to become a biological target for the prevention and treatment of pulmonary fibrosis in patients with sepsis-induced ARDS. At the same time, the expectation that ASLNC12002 and its related products may be used as clinical markers for the evaluation of early pulmonary fibrosis in ARDS patients should not be ignored.