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The role of p65 NF-kappaB/RelA in pancreatitis-induced Kupffer cell apoptosis.

Publication ,  Journal Article
Peng, Y; Gallagher, SF; Landmann, R; Haines, K; Murr, MM
Published in: J Gastrointest Surg
June 2006

Acute pancreatitis induces liver injury by upregulating Kupffer cell-derived Fas/FasL; on the other hand, acute pancreatitis induces apoptosis of Kupffer cells via NF-kappaB-dependent pathways. The balance between upregulation of Fas/FasL and Fas/FasL-induced apoptosis of its originator cell may determine the severity of pancreatitis-related liver injury. The aim of our study was to determine the role of p65 NF-kappaB/RelA in pancreatitis-induced Kupffer cell apoptosis. Acute pancreatitis was induced in NIH Swiss mice by a choline-deficient ethionine-supplement (CDE) diet. In vitro mouse Kupffer cell line was transfected with p65 siRNA and treated with pancreatic elastase to mimic pancreatitis. CDE pancreatitis upregulated nuclear translocation of p65 NF-kappaB/RelA, Fas/FasL, caspase-3, and DNA fragmentation in mice livers (all P < 0.001). In vitro, pancreatic elastase mimicked CDE-pancreatitis by upregulating nuclear translocation of p65 NF-kappaB/RelA, Fas/FasL, caspase-3, DNA fragmentation, and apoptosis in Kupffer cells (all P < 0.001). Transfection with p65 siRNA attenuated the elastase-induced nuclear translocation of p65 NF-kappaB/RelA, upregulation of Fas/FasL, caspase-3, DNA fragmentation, and apoptosis in Kupffer cells (all P < 0.001). Acute pancreatitis activates p65 NF-kappaB/RelA and induces apoptosis of Kupffer cells. Inhibition of p65NF-kappaB/RelA attenuates elastase-induced upregulation of proapoptotic pathways and apoptosis in Kupffer cells. The ability of Kupffer cells to autoregulate their stress response by inducing self-apoptosis warrants further investigation.

Duke Scholars

Published In

J Gastrointest Surg

DOI

ISSN

1091-255X

Publication Date

June 2006

Volume

10

Issue

6

Start / End Page

837 / 847

Location

United States

Related Subject Headings

  • fas Receptor
  • Up-Regulation
  • Tumor Necrosis Factors
  • Translocation, Genetic
  • Transfection
  • Transcription Factor RelA
  • Surgery
  • Reverse Transcriptase Polymerase Chain Reaction
  • Pancreatitis
  • Mice
 

Citation

APA
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ICMJE
MLA
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Peng, Y., Gallagher, S. F., Landmann, R., Haines, K., & Murr, M. M. (2006). The role of p65 NF-kappaB/RelA in pancreatitis-induced Kupffer cell apoptosis. J Gastrointest Surg, 10(6), 837–847. https://doi.org/10.1016/j.gassur.2005.12.013
Peng, Yanhua, Scott F. Gallagher, Regine Landmann, Krista Haines, and Michel M. Murr. “The role of p65 NF-kappaB/RelA in pancreatitis-induced Kupffer cell apoptosis.J Gastrointest Surg 10, no. 6 (June 2006): 837–47. https://doi.org/10.1016/j.gassur.2005.12.013.
Peng Y, Gallagher SF, Landmann R, Haines K, Murr MM. The role of p65 NF-kappaB/RelA in pancreatitis-induced Kupffer cell apoptosis. J Gastrointest Surg. 2006 Jun;10(6):837–47.
Peng, Yanhua, et al. “The role of p65 NF-kappaB/RelA in pancreatitis-induced Kupffer cell apoptosis.J Gastrointest Surg, vol. 10, no. 6, June 2006, pp. 837–47. Pubmed, doi:10.1016/j.gassur.2005.12.013.
Peng Y, Gallagher SF, Landmann R, Haines K, Murr MM. The role of p65 NF-kappaB/RelA in pancreatitis-induced Kupffer cell apoptosis. J Gastrointest Surg. 2006 Jun;10(6):837–847.
Journal cover image

Published In

J Gastrointest Surg

DOI

ISSN

1091-255X

Publication Date

June 2006

Volume

10

Issue

6

Start / End Page

837 / 847

Location

United States

Related Subject Headings

  • fas Receptor
  • Up-Regulation
  • Tumor Necrosis Factors
  • Translocation, Genetic
  • Transfection
  • Transcription Factor RelA
  • Surgery
  • Reverse Transcriptase Polymerase Chain Reaction
  • Pancreatitis
  • Mice