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1 Department of Surgery, Tufts-New England Medical Center and Tufts University School of Medicine, Boston, MA, USA
2 Department of Neuroscience, Tufts-New England Medical Center and Tufts University School of Medicine, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: gperides{at}tufts-nemc.org.
Supramaximal stimulation of the rat pancreas with cholecystokinin, or its analog caerulein,
triggers acute pancreatitis and a number of pancreatitis-associated acinar cell changes including
intracellular activation of digestive enzyme zymogens and acinar cell injury. It is generally
believed that some of these various acinar cell responses to supramaximal secretagogue
stimulation are inter-related and inter-dependent. In a recent report, Lu et al (Am J Physiol
285:G822-828, 2003) showed that secretin, by causing generation of cAMP and activation of
protein kinase A, sensitizes acinar cells to secretagogue-induced zymogen activation and, as a
result, submaximally stimulating concentrations of caerulein can, in the presence of secretin,
trigger intracellular zymogen activation. We find that secretin also sensitizes acinar cells to
secretagogue-induced cell injury and to sub-apical f-actin redistribution but that it does not alter
the caerulein concentration-dependence of other pancreatitis-associated changes such as
induction of a peak-plateau [Ca2+]i rise, inhibition of secretion, activation of ERK 1/2 and
activation of NF-
B. The finding that secretin sensitizes acinar cells to both intracellular
zymogen activation and cell injury is consistent with the concept that these two early events in
pancreatitis are closely inter-related and, possibly, inter-dependent. On the other hand, the
finding that, in the presence of secretin, caerulein can trigger sub-apical f-actin redistribution
without inhibiting secretion challenges the concept that disruption of the sub-apical f-actin web
is causally related to high-dose secretagogue-induced inhibition of secretion in pancreatic acinar
cells.
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