Abstract
Aims Our study aimed to investigate the role of long non-coding RNA ANRIL
(lnc-ANRIL) knock-down in regulating cell activities, inflammation and
downstream signaling pathways in mouse mesangial cellular diabetic nephropathy
(DN) model.
Methods The mouse mesangial cells (SV40-MES13 cells) were treated with
high-glucose (HG) to construct cellular DN model. Lnc-ANRIL knock-down plasmid
and control knock-down plasmid were transfected into HG-treated SV40-MES13 cells
as Sh-ANRIL group and Sh-NC group respectively.
Results Lnc-ANRIL expression was significantly higher in HG-treated
SV40-MES13 cells compared with normal glucose-treated SV40-MES13 cells and
osmotic control-treated SV40-MES13 cells. Lnc-ANRIL knock-down suppressed cell
proliferation and promoted cell apoptosis in HG-treated SV40-MES13 cells. As for
fibrosis, lnc-ANRIL knock-down reduced fibronectin and collagen I expressions in
HG-treated SV40-MES13 cells. Besides, the expressions of supernatant tumor
necrosis factor-alpha (TNF-α), monocyte chemoattractant protein-1
(MCP-1), interleukin (IL)-1β, IL-6, IL-8 and IL-18 were reduced in
Sh-ANRIL group compared with Sh-NC group. Furthermore, Wnt3, β-catenin,
p-MEK1 and p-ERK1 expressions were suppressed in Sh-ANRIL group compared with
Sh-NC group, which suggested that lnc-ANRIL knock-down inhibited
Wnt/β-catenin and MEK/ERK pathways in HG-treated
SV40-MES13 cells.
Conclusions Lnc-ANRIL knock-down suppresses mouse mesangial cell
proliferation, fibrosis, inflammation, Wnt/β-catenin and
MEK/ERK pathways in DN.
Microarray analysis reveals long non‑coding RNA SOX2OT as a novel candidate regulator in diabetic nephropathy
