mTOR contributes to ER stress and associated apoptosis in renal tubular cells

Guie Dong, Yu Liu, Lei Zhang, Shuang Huang, Han Fei Ding, Zheng Dong

Research output: Contribution to journalArticlepeer-review

38 Scopus citations


ER stress has been implicated in the pathogenesis of both acute and chronic kidney diseases. However, the molecular regulation of ER stress in kidney cells and tissues remains poorly understood. In this study, we examined tunicamycin-induced ER stress in renal proximal tubular cells (RPTC). Tunicamycin induced the phosphorylation and activation of PERK and eIF2α within 2 h in RPTC, which was followed by the induction of GRP78 and CHOP. Consistently, tunicamycin also induced apoptosis in RPTC. Interestingly, mTOR was activated rapidly during tunicamycin treatment, as indicated by phosphorylation of both mTOR and p70S6K. Inhibition of mTOR with rapamycin partially suppressed the phosphorylation of PERK and eIF2a and the induction of CHOP and GRP78 induction during tunicamycin treatment. Rapamycin also inhibited apoptosis during tunicamycin treatment and increased cell survival. Collectively, the results suggest that mTOR plays a regulatory role in ER stress, and inhibition of mTOR may have potential therapeutic effects in ER stress-related renal diseases.

Original languageEnglish (US)
Pages (from-to)F267-F274
JournalAmerican Journal of Physiology - Renal Physiology
Issue number3
StatePublished - 2015


  • Apoptosis
  • Endoplasmic reticulum stress
  • Mammmalian target of rapamycin
  • Renal tubular cells
  • Tunicamycin

ASJC Scopus subject areas

  • Physiology
  • Urology


Dive into the research topics of 'mTOR contributes to ER stress and associated apoptosis in renal tubular cells'. Together they form a unique fingerprint.

Cite this