Conclusion
Up-regulation of lncRNA GAS5 alleviates renal fibrosis in DN mice via down-regulation of miR-542-3p and up-regulation of ERBB4.
Methods
db/db mice were injected with lncRNA GAS5 high expression or miR-542-3p low expression related vectors. Biochemical experiments were performed to assess blood glucose level and urine protein concentration. HE, TUNEL and Masson stainings were employed to observe the cellular morphology, apoptosis, and fibrosis of renal tissues, respectively. ELISA was executed to examine the levels of IL-1β, IL-6, and TNF-α; and the superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) activities were evaluated. Bioinformatics analysis, dual-luciferase and RIP assays were performed to verify the relationship between lncRNA GAS5 and miR-542-3p, and miR-542-3p and ERBB4.
Objective
The present study was implemented to unravel the effect of lncRNA GAS5 on renal fibrosis induced by diabetic nephropathy (DN) by regulating the miR-542-3p/ERBB4 axis.
Results
LncRNA GAS5 and ERBB4 were lowly expressed and miR-542-3p was highly expressed in the renal tissues of DN mice. Overexpression of lncRNA GAS5 or low-expression of miR-542-3p diminished DN-induced renal fibrosis. LncRNA GAS5 could bind to miR-542-3p and miR-542-3p further modulating ERBB4 expression. Up-regulation of miR-542-3p neutralized the suppressive effect of lncRNA GAS5 overexpression and down-regulation of ERBB4 also counteracted the inhibitory impact of down-regulation of miR-542-3p on renal fibrosis in DN mice.