miR-29b inhibits LPS-induced apoptosis in human bronchial epithelial cell line 16HBE

Objective To study the effect of miR-29b on lipopolysaccharide(LPS)-induced apoptosis of human bronchial epithelial cell line 16HBE. Methods 16HBE cells were divided into control group, LPS group (LPS treatment), transfection mimics control group, transfection miR-29b mimics group. MTT assay for proliferation, flow cytometry was used for apoptosis; Western blot was used for checking the expression of cleaved cysteinyl aspartate specific proteins 3(c-caspase-3), cleaved cysteinyl aspartate specific proteinase 12(c-caspase-12), glucose-regulated protein 78(GRP78) and CCAAT/enhancer-binding protein C/EBP (CHOP) protein. Human bronchial epithelial cells 16HBE were co-transfected with miR-29b mimics and pcDNA-CHOP, the proliferation and apoptosis were also determined using the above method. Results Compared with the control group, the cell proliferation- activity and apoptosis rate of the LPS group decreased, and the protein expression level of c-caspase-3, c-caspase-12, GRP78, and CHOP all increased. Compared with the LPS+NC group, the LPS+miR-29b group showed an increased cell proliferation, decreased apoptosis and decreased expression of c-caspase-3, c-caspase-12, GRP78, and CHOP protein. pcDNA-CHOP reversed the effects of miR-29b mimics on the proliferation and apoptosis of bronchial epithelial cells under LPS conditions. Conclusions miR-29b inhibits 16HBE apoptosis induced by LPS; the mechanism might be related to the inhibition of endoplasmic reticulum stress.