Role of mitogen-activated protein kinases, NF-κB, and AP-1 on cerulein-induced IL-8 expression in pancreatic acinar cells

Don Ju Kyung, Hoon Yu Ji, Hye Young Kim, Hwan Kim Kyung

Research output: Chapter in Book/Report/Conference proceedingConference contribution

16 Citations (Scopus)

Abstract

The cholecystokine (CCK) analogue cerulein causes pathophysiological, morphological, and biochemical events similar to various aspects of human pancreatitis. Doses of CCK or cerulein beyond those that cause the maximum pancreatic secretion of amylase and lipase result in pancreatitis, which is characterized by a dysregulation of the digestive enzyme production and cytoplasmic vacuolization and the death of acinar cells, edema formation, and an infiltration of inflammatory cells into the pancreas. This study aims to investigate whether cerulein induces IL-8 expression in pancreatic acinar cells, and whether cerulein-induced IL-8 expression is inhibited in the cells transfected with mutant genes for c-jun (TAM-67), or IκBα (MAD-3) or treated inhibitors of mitogen-activated protein kinases (MAPKs). As a result, cerulein induced IL-expression, which was inhibited in the cells transfected with TAM-67 or MAD-3 or treated inhibitors of MAPK. In conclusion, activation of MAPK, nuclear factor-κB (NF-κB), and activator protein-1 (AP-1) may be the upstream signaling for cerulein-induced IL-8 expression in pancreatic acinar cells.

Original languageEnglish
Title of host publicationSignal Transduction Pathways, Part A
Subtitle of host publicationApoptotic and Extracellular Signalling
PublisherBlackwell Publishing Inc.
Pages368-374
Number of pages7
ISBN (Print)1573316458, 9781573316453
DOIs
Publication statusPublished - 2006 Jan 1

Publication series

NameAnnals of the New York Academy of Sciences
Volume1090
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

Fingerprint

Ceruletide
Acinar Cells
Transcription Factor AP-1
Mitogen-Activated Protein Kinases
Interleukin-8
Pancreatitis
jun Genes
Amylases
Lipase
Infiltration
Protein
Cells
Pancreas
Edema
Chemical activation
Enzymes

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

Cite this

Kyung, D. J., Ji, H. Y., Kim, H. Y., & Kyung, H. K. (2006). Role of mitogen-activated protein kinases, NF-κB, and AP-1 on cerulein-induced IL-8 expression in pancreatic acinar cells. In Signal Transduction Pathways, Part A: Apoptotic and Extracellular Signalling (pp. 368-374). (Annals of the New York Academy of Sciences; Vol. 1090). Blackwell Publishing Inc.. https://doi.org/10.1196/annals.1378.040
Kyung, Don Ju ; Ji, Hoon Yu ; Kim, Hye Young ; Kyung, Hwan Kim. / Role of mitogen-activated protein kinases, NF-κB, and AP-1 on cerulein-induced IL-8 expression in pancreatic acinar cells. Signal Transduction Pathways, Part A: Apoptotic and Extracellular Signalling. Blackwell Publishing Inc., 2006. pp. 368-374 (Annals of the New York Academy of Sciences).
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abstract = "The cholecystokine (CCK) analogue cerulein causes pathophysiological, morphological, and biochemical events similar to various aspects of human pancreatitis. Doses of CCK or cerulein beyond those that cause the maximum pancreatic secretion of amylase and lipase result in pancreatitis, which is characterized by a dysregulation of the digestive enzyme production and cytoplasmic vacuolization and the death of acinar cells, edema formation, and an infiltration of inflammatory cells into the pancreas. This study aims to investigate whether cerulein induces IL-8 expression in pancreatic acinar cells, and whether cerulein-induced IL-8 expression is inhibited in the cells transfected with mutant genes for c-jun (TAM-67), or IκBα (MAD-3) or treated inhibitors of mitogen-activated protein kinases (MAPKs). As a result, cerulein induced IL-expression, which was inhibited in the cells transfected with TAM-67 or MAD-3 or treated inhibitors of MAPK. In conclusion, activation of MAPK, nuclear factor-κB (NF-κB), and activator protein-1 (AP-1) may be the upstream signaling for cerulein-induced IL-8 expression in pancreatic acinar cells.",
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Kyung, DJ, Ji, HY, Kim, HY & Kyung, HK 2006, Role of mitogen-activated protein kinases, NF-κB, and AP-1 on cerulein-induced IL-8 expression in pancreatic acinar cells. in Signal Transduction Pathways, Part A: Apoptotic and Extracellular Signalling. Annals of the New York Academy of Sciences, vol. 1090, Blackwell Publishing Inc., pp. 368-374. https://doi.org/10.1196/annals.1378.040

Role of mitogen-activated protein kinases, NF-κB, and AP-1 on cerulein-induced IL-8 expression in pancreatic acinar cells. / Kyung, Don Ju; Ji, Hoon Yu; Kim, Hye Young; Kyung, Hwan Kim.

Signal Transduction Pathways, Part A: Apoptotic and Extracellular Signalling. Blackwell Publishing Inc., 2006. p. 368-374 (Annals of the New York Academy of Sciences; Vol. 1090).

Research output: Chapter in Book/Report/Conference proceedingConference contribution

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N2 - The cholecystokine (CCK) analogue cerulein causes pathophysiological, morphological, and biochemical events similar to various aspects of human pancreatitis. Doses of CCK or cerulein beyond those that cause the maximum pancreatic secretion of amylase and lipase result in pancreatitis, which is characterized by a dysregulation of the digestive enzyme production and cytoplasmic vacuolization and the death of acinar cells, edema formation, and an infiltration of inflammatory cells into the pancreas. This study aims to investigate whether cerulein induces IL-8 expression in pancreatic acinar cells, and whether cerulein-induced IL-8 expression is inhibited in the cells transfected with mutant genes for c-jun (TAM-67), or IκBα (MAD-3) or treated inhibitors of mitogen-activated protein kinases (MAPKs). As a result, cerulein induced IL-expression, which was inhibited in the cells transfected with TAM-67 or MAD-3 or treated inhibitors of MAPK. In conclusion, activation of MAPK, nuclear factor-κB (NF-κB), and activator protein-1 (AP-1) may be the upstream signaling for cerulein-induced IL-8 expression in pancreatic acinar cells.

AB - The cholecystokine (CCK) analogue cerulein causes pathophysiological, morphological, and biochemical events similar to various aspects of human pancreatitis. Doses of CCK or cerulein beyond those that cause the maximum pancreatic secretion of amylase and lipase result in pancreatitis, which is characterized by a dysregulation of the digestive enzyme production and cytoplasmic vacuolization and the death of acinar cells, edema formation, and an infiltration of inflammatory cells into the pancreas. This study aims to investigate whether cerulein induces IL-8 expression in pancreatic acinar cells, and whether cerulein-induced IL-8 expression is inhibited in the cells transfected with mutant genes for c-jun (TAM-67), or IκBα (MAD-3) or treated inhibitors of mitogen-activated protein kinases (MAPKs). As a result, cerulein induced IL-expression, which was inhibited in the cells transfected with TAM-67 or MAD-3 or treated inhibitors of MAPK. In conclusion, activation of MAPK, nuclear factor-κB (NF-κB), and activator protein-1 (AP-1) may be the upstream signaling for cerulein-induced IL-8 expression in pancreatic acinar cells.

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BT - Signal Transduction Pathways, Part A

PB - Blackwell Publishing Inc.

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Kyung DJ, Ji HY, Kim HY, Kyung HK. Role of mitogen-activated protein kinases, NF-κB, and AP-1 on cerulein-induced IL-8 expression in pancreatic acinar cells. In Signal Transduction Pathways, Part A: Apoptotic and Extracellular Signalling. Blackwell Publishing Inc. 2006. p. 368-374. (Annals of the New York Academy of Sciences). https://doi.org/10.1196/annals.1378.040