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Role of Mitogen‐Activated Protein Kinases, NF‐κB, and AP‐1 on Cerulein‐Induced IL‐8 Expression in Pancreatic Acinar Cells
Author(s) -
JU KYUNG DON,
YU JI HOON,
KIM HYEYOUNG,
KIM KYUNG HWAN
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1378.040
Subject(s) - mapk/erk pathway , ceruletide , kinase , protein kinase a , pancreas , activator (genetics) , medicine , endocrinology , chemistry , transfection , pancreatitis , acinus , acute pancreatitis , microbiology and biotechnology , biology , cancer research , cholecystokinin , gene , biochemistry , receptor
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.