PRMT6 relieves lipopolysaccharide-induced lung bronchial epithelial cell injury by inhibiting the PTEN/β-catenin pathway

Objective To explore the effect of protein arginine methyltransferase 6 (PRMT6) on lipopolysaccharide (LPS)-induced lung bronchial epithelial cell injury and its possible mechanism. Methods Human bronchial epithelial cell line 16HBE was cultured in vitro, and the expression of PRMT6 mRNA was detected by qRT-PCR. The expression of PRMT6, phosphatase and tensin homolog (PTEN), p-β-catenin and β-catenin was detected by Western blot. Cell viability was detected by CCK-8. Cell apoptosis and ROS production were detected by flow cytometry. The contents of interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α and malondialdehyde (MDA), as well as SOD and lactate dehydrogenase (LDH) activities in the supernatant of cell culture was detected. Results LPS inhibited the expression of PRMT6 mRNA and protein in cells in a dose-dependent manner. Compared with the blank control group, the LPS group showed significantly decreases in the expression of PRMT6 mRNA and protein, the expression of p-β-catenin/β-catenin protein (P<0.05), decreases in cell viability and SOD activity (P<0.05), and increases in the expression of PTEN protein, apoptosis rate, the contents of ROS, MDA, IL-1β, IL-6 and TNF-α, and LDH activity (P<0.05). Compared with the LPS group, there was no statistically significant differences in the indicators of the LPS+oe-NC group (P>0.05). Compared with the LPS+oe-NC group, the LPS+oe-PRMT6 group presented remarkable increases in the expression of PRMT6 mRNA and protein, the expression of p-β-catenin/β-catenin protein (P＜0.05), increases in cell viability and SOD activity (P＜0.05), and decreases in the expression of PTEN protein, apoptosis rate, the contents of ROS, MDA, IL- 1β, IL-6 and TNF-α, and LDH activity (P＜0.05). Compared with the LPS+oe-PRMT6 group, the LPS+oe-PRMT6+oe-PTEN group showed the expression of PRMT6 without significant difference (P>0.05),remarkable decreases in the expression of p-β-catenin/β-catenin protein (P＜0.05), decreases in cell viability and SOD activity (P＜0.05), and increases in the expression of PTEN protein, apoptosis rate, the contents of ROS, MDA, IL-1β, IL-6 and TNF-α, and LDH activity (P<0.05). Conclusions PRMT6 can improve lung bronchial epithelial cell injury induced by LPS by inhibiting the PTEN/β-catenin pathway.