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Nuclear factor kappa B–dependent gene transcription in cholecystokinin- and tumor necrosis factor-α–stimulated isolated acinar cells is regulated by p38 mitogen-activated protein kinase
Journal article   Peer reviewed

Nuclear factor kappa B–dependent gene transcription in cholecystokinin- and tumor necrosis factor-α–stimulated isolated acinar cells is regulated by p38 mitogen-activated protein kinase

Deborah E Williard, Erik Twait, Zuobiao Yuan, A. Brent Carter and Isaac Samuel
The American journal of surgery, Vol.200(2), pp.283-290
2010
DOI: 10.1016/j.amjsurg.2009.12.004
PMID: 20413104
url
https://www.ncbi.nlm.nih.gov/pmc/articles/2910146View
Open Access

Abstract

Mitogen-activated protein (MAP) kinases and nuclear factor kappa B (NF-κB) are implicated in early stages of acute pancreatitis pathogenesis. We investigated the relationship between the p38 MAP kinase and NF-κB in isolated acinar cells. Isolated rodent acinar cells were stimulated with agonists after infection with an adenovector containing a luciferase promoter driven only by NF-κB and an adenovector containing the dominant negative (DN) form of p38 (empty vector in controls). Initial immunoblots confirmed that the agonist stimulated p38 activation in acinar cells was substantially attenuated by DN p38 overexpression. Stimulation of native cholecystokinin (CCK)-A receptors or tumor necrosis factor-α (TNF-α) receptors promoted a significant increase in NF-κB-dependent gene transcription in cells infected with the empty vector, while overexpression of DN p38 significantly abrogated NF-κB-dependent luciferase activity. These findings support our hypothesis that p38 is involved in the activation of proinflammatory nuclear transcription factors such as NF-κB in pancreatic exocrine cells.
 NF-κB Acute pancreatitis Rat Mouse p38 TNF-α Adenoviral vector MAP kinase CCK Acinar cell

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