In:
American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 276, No. 2 ( 1999-02-01), p. G499-G506
Abstract:
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 (Ras N17 ) was utilized. Isolated acini were infected with various titers of either a control adenovirus or an adenoviral construct expressing Ras N17 for 24 h before being treated with CCK. Titer-dependent expression of Ras N17 in the acini was confirmed by Western blotting. Infection with control adenovirus [10 6 –10 9 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 ras N17 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.
Type of Medium:
Online Resource
ISSN:
0193-1857
,
1522-1547
DOI:
10.1152/ajpgi.1999.276.2.G499
Language:
English
Publisher:
American Physiological Society
Publication Date:
1999
detail.hit.zdb_id:
1477329-6
SSG:
12
