PKD prevents H2O2-induced apoptosis via NF-κB and p38 MAPK in RIE-1 cells

Jun Song, Jing Li, Jingbo Qiao, Sunil Jain, B. Mark Evers, Dai H. Chung

Research output: Contribution to journalArticlepeer-review

39 Scopus citations


Previously, we demonstrated that protein kinase D (PKD) plays a protective role during H2O2-induced intestinal cell death. Here, we sought to determine whether this effect is mediated by nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs). Treatment with H2O2 activated NF-κB in RIE-1 cells; H2O2 also induced the translocation of NF-κB p65 as well as phosphorylation of IκB-α. PKD1 siRNA inhibited H2O2-induced activation, translocation of NF-κB, and phosphorylation of IκB-α. We also found that overexpression of wild type PKD1 attenuated H2O2-induced phosphorylation of p38 MAPK and its upstream activator, MAPK kinase (MKK) 3/6, whereas the phosphorylation was increased by PKD1 siRNA or kinase-dead PKD1. Phosphorylation of neither extracellular signal-regulated kinases (ERK) 1/2 nor c-Jun N-terminal kinases (JNK) was altered by PKD1 plasmids or siRNA. Our findings suggest that PKD protects intestinal cells through up-regulation of NF-κB and down-regulation of p38 MAPK.

Original languageEnglish (US)
Pages (from-to)610-614
Number of pages5
JournalBiochemical and Biophysical Research Communications
Issue number3
StatePublished - Jan 16 2009


  • NF-κB
  • Oxidative stress
  • Protein kinase D
  • p38 MAPK

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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