Mechanism of long non-coding RNA uc.412 in mediating the autophagy of mesangial cells induced by transforming growth factor-β1

Objective To explore the mechanism of long non-coding RNA uc.412 (LncRNA uc.412) in mediating the autophagy of mesangial cells induced by transforming growth factor-β1 (TGF-β1). Methods Rat mesangial cells were treated with TGF-β1 (10 μg/L). The expression of autophagy markers LC3 and p62 were detected by Western blot. The expression of Lnc RNA uc.412 was detected by Real-time PCR. The mesangial cells infected with over-expressed LncRNA uc.412 lentivirus were used, and the infection efficiency was detected by Real-time PCR. Then, Western blot and Real-time PCR were used to detect the expression of LC3 and p62 at protein and mRNA levels. The mesangial cells were treated with TGF-β1 (10 μg/L) and SIS3, a specific phosphorylation inhibitor of Smad3 (1 μmol). Western blot was used to detect the expression of pSmad3 protein, while Real-time PCR to detect the expression of LncRNA uc.412. Results Compared with the control group, the TGF-β1 group showed an up-regulated ratio of LC3 Ⅱ to LC3Ⅰand increased expression of p62 and LncRNA uc.412 (P<0.05). The levels of LC3 and p62 at protein and mRNA levels were higher in the LncRNA uc.412 over-expression group than those in the control and vector groups (P<0.05). Compared with the control group, the amounts of pSmad3 and LncRNA uc.412 was up-regulated in the TGF-β1 group (P<0.05). Compared with the TGF-β1 group, the amounts of pSmad3 and LncRNA uc.412 was down-regulated in the TGF-β1+SIS3 group (P<0.05). Conclusions LncRNA uc.412 can act as a downstream effector molecule of the TGF/Smad3 pathway to promote mesangial cell autophagy, which provides new thought for the prevention and treatment of chronic kidney disease.