PKD prevents H{sub 2}O{sub 2}-induced apoptosis via NF-{kappa}B and p38 MAPK in RIE-1 cells

Journal Article · Fri Jan 16 04:00:00 EST 2009 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/j.bbrc.2008.11.106· OSTI ID:21255841

Jun, Song ^[1]; Jing, Li ^[1]; Jingbo, Qiao ^[1]; Jain, Sunil ^[2]; Mark Evers, B ^[1]; Chung, Dai H ^[1]

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1. Department of Surgery, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-0353 (United States)
2. Department of Pediatrics, University of Texas Medical Branch, Galveston, TX 77555 (United States)

Previously, we demonstrated that protein kinase D (PKD) plays a protective role during H{sub 2}O{sub 2}-induced intestinal cell death. Here, we sought to determine whether this effect is mediated by nuclear factor-{kappa}B (NF-{kappa}B) and mitogen-activated protein kinases (MAPKs). Treatment with H{sub 2}O{sub 2} activated NF-{kappa}B in RIE-1 cells; H{sub 2}O{sub 2} also induced the translocation of NF-{kappa}B p65 as well as phosphorylation of I{kappa}B-{alpha}. PKD1 siRNA inhibited H{sub 2}O{sub 2}-induced activation, translocation of NF-{kappa}B, and phosphorylation of I{kappa}B-{alpha}. We also found that overexpression of wild type PKD1 attenuated H{sub 2}O{sub 2}-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-{kappa}B and down-regulation of p38 MAPK.

• OSTI ID: 21255841
• Journal Information: Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 3 Vol. 378; ISSN 0006-291X; ISSN BBRCA9
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
APOPTOSIS
CHROMOSOMAL ABERRATIONS
GENE REGULATION
HYDROGEN PEROXIDE
OXIDATION
PHOSPHORYLATION
PHOSPHOTRANSFERASES
PLASMIDS
SIGNALS
STRESSES