Visit our Expo - Redox and Inflammation signaling 2012

Session XIV : Transcriptional and translational control Poster XIV, 33
NF-kB, AP-1 and mitogen-activated protein kinase in chemokine expression in
pancreatic Acinar cells.
Kyung Don Ju, Ji Hoon Yu, Kyung Hwan Kim and Hyeyoung Kim*
Department of Pharmacology, Brain Korea 21 Project for Medical Science, Yonsei
University College of Medicine, Seoul 120-752, Korea,E-mail:clock1375@paran.com
Cholecystokine(CCK) analogue cerulein causes pathophysiological, morphological and
biochemical similarities to various aspects of human pancreatitis. Doses of CCK or cerulein
beyond those that cause the maximum pancreatic secretion of amylase and lipase results 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. Present study aims to investigate whether cerulein
induced NF-kB and AP-1 activation, MAPK phosphorylation and the expression of MCP-1 in
pancreatic acinar cells, and whether these alterations were inhibited by transfection of I-kB
mutant, c-jun dominant negative and inhibitors of MAPK. As a result, cerulein induced NFkB,
AP-1 activation, MAPK phosphorylation and induction of chemokines(IL-8, MCP-1)
expression in the cells. Both transfection of I-kB mutant, c-jun dominant negative and
inhibitors of MAPK inhibited cerulein-induced chemokines in acinar cells. In conclusion,
cerulein activates NF-kB, AP-1 and MAPK resulting in upregulation of inflammatory MCP-1
expression in acinar cells. Inhibition of NF-kB, AP-1 and MAPK might alleviate the
inflammatory response in pancreatic acinar cells by suppressing chemokine expression.
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