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Am J Physiol Gastrointest Liver Physiol 279: G827-G836, 2000;
0193-1857/00 $5.00
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Vol. 279, Issue 4, G827-G836, October 2000

p53-Dependent acinar cell apoptosis triggers epithelial proliferation in duct-ligated murine pancreas

Charles R. Scoggins, Ingrid M. Meszoely, Michihiko Wada, Anna L. Means, Liying Yang, and Steven D. Leach

Departments of Surgery and Cell Biology, The Vanderbilt-Ingram Cancer Center and Nashville Veterans Affairs Medical Center, Vanderbilt University, Nashville, Tennessee 37232-2736

The mechanisms linking acinar cell apoptosis and ductal epithelial proliferation remain unknown. To determine the relationship between these events, pancreatic duct ligation (PDL) was performed on p53(+/+) and p53(-/-) mice. In mice bearing a wild-type p53 allele, PDL resulted in upregulation of p53 protein in both acinar cells and proliferating duct-like epithelium. In contrast, upregulation of Bcl-2 occurred only in duct-like epithelium. Both p21WAF1/CIP1 and Bax were also upregulated in duct-ligated lobes. After PDL in p53(+/+) mice, acinar cells underwent widespread apoptosis, while duct-like epithelium underwent proliferative expansion. In the absence of p53, upregulation of p53 target genes and acinar cell apoptosis did not occur. The absence of acinar cell apoptosis in p53(-/-) mice also eliminated the proliferative response to duct ligation. These data demonstrate that PDL-induced acinar cell apoptosis is a p53-dependent event and suggest a direct link between acinar cell apoptosis and proliferation of duct-like epithelium in duct-ligated pancreas.

duct ligation; regeneration; Bcl-2; Bax; p21


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