Next Article in Journal
Se-Methylselenocysteine Inhibits Apoptosis Induced by Clusterin Knockdown in Neuroblastoma N2a and SH-SY5Y Cell Lines
Next Article in Special Issue
Lidocaine Sensitizes the Cytotoxicity of Cisplatin in Breast Cancer Cells via Up-Regulation of RARβ2 and RASSF1A Demethylation
Previous Article in Journal
Dexamethasone Improves Heat Stroke-Induced Multiorgan Dysfunction and Damage in Rats
Previous Article in Special Issue
Squamosamide Derivative FLZ Protects Retinal Pigment Epithelium Cells from Oxidative Stress through Activation of Epidermal Growth Factor Receptor (EGFR)-AKT Signaling
Article Menu
Issue 11 (November) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2014, 15(11), 21314-21330; doi:10.3390/ijms151121314

Inhibition of p53 deSUMOylation Exacerbates Puromycin Aminonucleoside-Induced Apoptosis in Podocytes

1
Department of Nephrology, Liaoning Translational Medicine Center of Nephrology, the First Affiliated Hospital of Dalian Medical University, Dalian 116011, China
2
Department of Nephrology, State Key Laboratory of Kidney Disease, PLA General Hospital, Beijing 100853, China
*
Author to whom correspondence should be addressed.
Received: 8 September 2014 / Revised: 4 November 2014 / Accepted: 5 November 2014 / Published: 18 November 2014
(This article belongs to the Collection Programmed Cell Death and Apoptosis)
View Full-Text   |   Download PDF [4642 KB, uploaded 18 November 2014]   |  

Abstract

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’s lymphoma 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 puromycin aminonucleoside (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 deSUMOylation may provide a novel strategy for the treatment of glomerular disorders that involve podocyte apoptosis. View Full-Text
Keywords: apoptosis; deSUMOylation; p53; podocyte; sentrin/SUMO-specific protease 1 apoptosis; deSUMOylation; p53; podocyte; sentrin/SUMO-specific protease 1
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Wang, L.; Zhu, J.; Fang, M.; Zhang, T.; Xie, H.; Wang, N.; Shen, N.; Guo, H.; Fu, B.; Lin, H. Inhibition of p53 deSUMOylation Exacerbates Puromycin Aminonucleoside-Induced Apoptosis in Podocytes. Int. J. Mol. Sci. 2014, 15, 21314-21330.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top