ABSTRACT
Objective:To explore the effects of LncRNA HCG18 on endoplasmic reticulum stress and autophagy via regulating miR-185-5p/AGER axis in diabetic nephropathy (DN) .Methods:The kidney tissues of patients with DN were collected and the podocyte injury model induced by high glucose (HG) was established. The expression of HCG18 in renal tissue in DN patients and cell model was detected. The localization and expression of HCG18 in cells were determined. The regulatory relationship between HCG18 and miR-185-5p, miR-185-5p and AGER was testified. QRT-PCR and western blot were used to detect the expression of endoplasmic reticulum stress related factors (CHOP, XBP1) and autophagy related factors (Beclin-1, p62) .Results:Compared with non-DN patients, HCG18 was overexpressed in renal tissue of DN patients ( P<0.05) . Compared with normal glucose (NG) group, mRNA and protein expression of endoplasmic reticulum stress related factors (CHOP, XBP1) were overexpressed but mRNA and protein expression of autophagy related factors Beclin-1 were inhibited, p62 mRNA and protein expression were increased (all P<0.05) . HCG18 regulated the miR-185-5p/AGER axis and played a biological role. Knocking down of HCG18 reduced endoplasmic reticulum stress, activated autophagy and reduced podocyte injury, but this effect can be partially reversed by miR-185-5p inhibitors. Conclusion:HCG18 regulates the miR-185-5p/AGER signal axis and promotes DN progression through regulating endoplasmic reticulum stress and autophagy.