The cytoprotective role of autophagy in puromycin aminonucleoside treated human podocytes

Yu-Lin Kang, Moin Ahson Saleem, Kwok Wah Chan, Benjamin Yat-Ming Yung, Helen Ka-Wai Law

Research output: Contribution to journalArticle (Academic Journal)peer-review

12 Citations (Scopus)

Abstract

Autophagy is a ubiquitous catabolic process involving degradation of damaged organelles and protein aggregates. It shows cytoprotective effects in many cell types and helps to maintain cell homeostasis. In many glomerular diseases, podocyte damage leads to the disruption of the renal filtration barrier and subsequent proteinuria. Puromycin aminonucleoside (PAN) which induces podocyte apoptosis in vitro and in vivo is widely used for studying the pathophysiology of glomerular diseases. It has been shown that PAN induces autophagy in podocytes. However, the relationship between autophagy and apoptosis in PAN treated human podocytes is not known and the role of PAN-induced autophagy in podocyte survival remains unclear. Here we demonstrate that PAN induced autophagy in human podocytes prior to apoptosis which was featured with the activation of mTOR complex 1 (mTORC1). When the PAN-induced autophagy was inhibited by 3-methyladenine (3-MA) or chloroquine (CQ), podocyte apoptosis increased significantly along with the elevation of active caspase-3. Under such circumstance, the podocyte cytoskeleton was also disrupted. Collectively, our results suggested that the induced autophagy may be an early adaptive cytoprotective mechanism for podocyte survival after PAN treatment.

Original languageEnglish
Pages (from-to)628-34
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume443
Issue number2
DOIs
Publication statusPublished - 10 Jan 2014

Keywords

  • Autophagy
  • Cell Line
  • Cytoprotection
  • Cytoskeleton
  • Dose-Response Relationship, Drug
  • Humans
  • Podocytes
  • Puromycin Aminonucleoside
  • Journal Article
  • Research Support, Non-U.S. Gov't

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