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Am J Physiol Gastrointest Liver Physiol 276: G499-G506, 1999;
0193-1857/99 $5.00
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Vol. 276, Issue 2, G499-G506, February 1999

Adenovirus-mediated gene transfer of RasN17 inhibits specific CCK actions on pancreatic acinar cells

Barbara Nicke, Min-Jen Tseng, Marycarol Fenrich, and Craig D. Logsdon

Department of Physiology, University of Michigan, Ann Arbor, Michigan 48109-0622

CCK stimulates pleiotrophic responses in pancreatic acinar cells; however, the intracellular signaling pathways involved are not well understood. To evaluate the role of the ras gene product in CCK actions, a strategy involving in vitro adenoviral-mediated gene delivery of a dominant-negative mutant Ras (RasN17) was utilized. Isolated acini were infected with various titers of either a control adenovirus or an adenoviral construct expressing RasN17 for 24 h before being treated with CCK. Titer-dependent expression of RasN17 in the acini was confirmed by Western blotting. Infection with control adenovirus [106-109 plaque-forming units/mg acinar protein (multiplicity of infection of ~1-1,000)] had no effect on CCK stimulation of acinar cell amylase release, extracellular-regulated kinase (ERK) or c-Jun kinase (JNK) kinases, or DNA synthesis. In contrast, infection with adenovirus bearing rasN17 increased basal amylase release, inhibited CCK-mediated JNK activation, had no effect on CCK activation of ERK, and inhibited DNA synthesis. These data demonstrate important roles for Ras in specific actions of CCK on pancreatic acinar function.

cell proliferation; mitogen-activated protein kinase; c-Jun kinase; secretion


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