Nuclear factor kappa B–dependent gene transcription in cholecystokinin- and tumor necrosis factor-⍺–stimulated isolated acinar cells is regulated by p38 mitogen-activated protein kinase - 19/08/11
Corresponding author. Tel.: +1-319-356-7359; fax: +1-319-356-8378Abstract |
Background |
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.
Methods |
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).
Results |
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-⍺ (TNF-⍺) 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.
Conclusions |
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.
Le texte complet de cet article est disponible en PDF.Keywords : MAP kinase, Acinar cell, Acute pancreatitis, Rat, Mouse, p38, NF-κB, CCK, TNF-⍺, Adenoviral vector
Plan
Vol 200 - N° 2
P. 283-290 - août 2010 Retour au numéro
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