Volume 30, Issue 2, 2021
DOI: 10.24205/03276716.2020.4069
LncRNA TUG1 affects the inflammatory factors and apoptosis of glomerular mesangial cells through targeting the miR-16-5p regulated cGAS-STING pathway in mice with lupus nephritis
Abstract
Our study intends to investigate the effect and mechanisms of lncRNA TUG1 on the inflammatory factors secretion and apoptosis of glomerular mesangial cells of mice with lupus nephritis. lncRNA TUG1 in glomerular mesangial cells from normal or lupus nephritis mice were knocked down with siRNA followed by measuring TUG1 and miR-16-5p expression by RT-qPCR and TNF-?, IL-1?, IL-6, cGAS, STING, and TBK1 protein expression by Western blot and cell apoptosis by flow cytometry. The online bioinformatics database and dual-luciferase reporting system assessed the relationship between TUG1 and miR-16-5p. Compared with normal mesangial cells, TUG1 was up-regulated and miR-16-5p expression was decreased in LN glomerular mesangial cells. Knockdown of TUG1 or miR-16-5p overexpression inhibited TNF-?, IL-1?, and IL-6 secretion and promoted apoptosis. miR-16-5p inhibition reversed the TUG1’s effect on apoptosis, cGAS-STING pathway, and TNF-?, IL-1?, and IL-6 secretion in glomerular mesangial cells. cGAS-STING pathway activator CDN reversed miR-16-5p and TUG1’s effect on inflammatory factors and apoptosis of glomerular mesangial cells. In conclusion, TUG1 can promote the production of inflammatory factors and inhibit glomerular mesangial cells apoptosis via miR-16-5p-regulated cGAS-STING signaling.
Keywords
lncRNA TUG1; miR-16-5p; cGAS - STING pathways; lupus nephritis