MiR-222-3p ameliorates glucocorticoid-induced inhibition of airway epithelial cell repair through down-regulating GILZ expression

Tectorigenin regulates migration, invasion, and apoptosis in dexamethasone‐induced human airway epithelial cells through up‐regulating miR‐222‐3p

“…It has been found that both adult and children asthmatics have damage and shedding of airway epithelial cells, and that endobronchial biopsies have confirmed that almost all asthmatics show varying degrees of airway epithelial damage, which may further intensify asthmatic inflammation (Barbato et al, 2006; Dorscheid et al, 2001; Park et al, 2015). At present, Dex as one of GCs is widely used in asthma treatment, but relevant studies demonstrated that Dex can also hinder the repair of cells through inhibiting the proliferation of epithelial cells (He et al, 2020). To verify the effects of Dex and Tectorigenin on airway epithelial cells, we used Dex, Tectorigenin, and Dex combined with Tectorigenin to treat 9HTE cells in vitro.…”

“…MicroRNAs (miRs) are small RNAs that do not encode for proteins and play crucial roles in regulating many important physiological processes of cells (Xiong et al, 2019; Zhao et al, 2018). These studies have shown that miR‐145‐5p was up‐regulated in asthma pathogenesis and it is one of the biomarkers of respiratory diseases; miR‐328 play an important role in the regulation of wound repair by participating in the actin pathway; miR‐888 and miR‐342‐5p also are associated with the regulation of wound repair process in the airway epithelial; miR‐222‐3p is involved in a variety of physiological and pathological processes of cells, such as repairing GCs‐induced airway epithelial injury by down‐regulating GC‐induced leucine zipper expression (He et al, 2020; Liu et al, 2014; Narozna et al, 2017; Xiong et al, 2019). However, whether Tectorigenin can regulate the repair of GCs‐induced airway epithelial injury in asthma by regulating certain miRs still requires further study.…”

“…Studies have shown that the activation of MAPK signaling pathway, which can regulate cell proliferation, migration, and apoptosis around injured site, plays a key role in the repair process after airway epithelial injury (Jia et al, 2018; Jiang et al, 2017; Jiang & Tang, 2015). Raf1 is an upstream signaling molecule of MAPK cascade reaction, and can act phosphorylate and activate mitogen‐activated protein kinase (MEK), which further phosphorylate and activates ERK, thereby mediating cell survival, proliferation, and differentiation (He et al, 2020). It has revealed that specific inhibitors of MEK1/2 and ERK1/2 in the MAPK/ERK pathway markedly inhibit the repair of airway epithelium injury (Lind et al, 2006; Wadsworth et al, 2006).…”

“…Dex significantly inhibited the phosphorylation of Raf‐1 in murine thymocytes (Ayroldi et al, 2002). Furthermore, Dex can inhibit the activation of MAPK pathway by inhibiting the phosphorylation of MEK1/2, Raf1, and ERK1/2 in 9HTE cells, and then inhibit cell proliferation and migration in turn (He et al, 2020). Therefore, MAPK pathway may play an important role in Dex's regulation of airway epithelial injury.…”

miRNAs as Modern Biomarkers in Asthma Therapy

“…The introduction of miRNA-222-3p led to a different therapeutic effect than that of steroids; a decrease in GILZ, promotion of the phosphorylation of signaling factors, and the activation of MAPK. The effect of these actions may be to promote repair of the damaged airway epithelium after using miRNA-222-3p [74]. Table 1 below summarizes the results of the studies presented above.…”