Abstract: FR-PO708

Inhibition of p53 Desumoylation by SENP1 Exacerbates Puromycin Aminonucleoside-Induced Apoptosis in Podocytes

Session Information

Category: Glomerular

  • 1002 Glomerular: Basic/Experimental Pathology


  • Wang, Lingyu, the First Affiliated Hospital of Dalian Medical University, Dalian, China

Apoptosis is a major cause of reduced podocyte numbers, which leads to proteinuria and/or glomerulosclerosis. Emerging evidence has indicated that deSUMOylation, a dynamic post-translational modification that reverses SUMOylation, is involved in the apoptosis of Burkitt’slymphoma cells and cardiomyocytes; however, the impact of deSUMOylation on podocyte apoptosis remains unexplored. The p53 protein plays a major role in the pathogenesis of podocyte apoptosis, and p53 can be SUMOylated.


Therefore, in the present study, we evaluated the effect of p53 deSUMOylation, which is regulated by sentrin/SUMO-specific protease 1 (SENP1), on podocyte apoptosis.


Our results showed that SENP1 deficiency significantly increases PAN-induced podocyte apoptosis. Moreover, SENP1 knockdown results in the accumulation of SUMOylated p53 protein and the increased expression of the p53 target pro-apoptotic genes, BAX, Noxa and PUMA, in podocytes during PAN stimulation.


Thus, SENP1 may be essential for preventing podocyte apoptosis, at least partly through regulating the functions of p53 protein via deSUMOylation. The regulation of deSUMOylationmay provide a novel strategy for the treatment of glomerular disorders that involve podocyte apoptosis.