The Lnc-Gm20716/miR-20b-5p/ULK1 axis regulates HDM-induced endoplasmic reticulum stress and Golgi fragmentation in mouse bronchial epithelial cells.

Asthma is a chronic inflammatory disease affecting bronchi, and it is a global challenge to find an effective treatment for this disease. Lnc-Gm20716 is significantly expressed in cases of bronchial epithelial cell injury. Furthermore, studies indicate that ULK1 is implicated in the development of inflammatory diseases. Through both in vivo and in vitro experiments, it has been elucidated that Lnc-Gm20716/miRNA-20b-5p influences endoplasmic reticulum stress and Golgi fragmentation in asthmatic bronchial epithelial cells via the ULK1 signaling axis. The intracellular localization of Lnc-Gm20716 was assessed using FISH. A lentivirus designed to silence Lnc-Gm20716 was employed to infect primary mouse bronchial epithelial cells (MBECs). GO analysis was conducted to evaluate the specific effects of Lnc-Gm20716, revealing that it contributes to HDM-induced endoplasmic reticulum stress and fragmentation of the Golgi apparatus in MBECs, as determined through Western Blot and immunofluorescence techniques. Bioinformatics tools were utilized to identify potential targets of Lnc-Gm20716, and subsequent experiments, including qRT-PCR, luciferase reporter assays, and anti-AGO2 RIP, confirmed that miR-20b-5p acts as a molecular sponge for Lnc-Gm20716. Furthermore, ULK1 is a direct target of miR-20b-5p in MBECs. In summary, the down-regulation of Lnc-Gm20716 enhances the alleviation of endoplasmic reticulum stress and Golgi fragmentation in HDM-induced MBECs. Within these cells, Lnc-Gm20716 functions as a molecular sponge for miR-20b-5p, with ULK1 identified as a direct target of miR-20b-5p. The inhibition of ULK1 significantly mitigates endoplasmic reticulum stress and Golgi fragmentation in MBECs.