Acinar cell apoptosis and the origin of tubular complexes in caerulein-induced pancreatitis

Citation
Le. Reid et Ni. Walker, Acinar cell apoptosis and the origin of tubular complexes in caerulein-induced pancreatitis, INT J EXP P, 80(4), 1999, pp. 205-215
Citations number
45
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY
ISSN journal
09599673 → ACNP
Volume
80
Issue
4
Year of publication
1999
Pages
205 - 215
Database
ISI
SICI code
0959-9673(199908)80:4<205:ACAATO>2.0.ZU;2-9
Abstract
The interrelationship between acinar cell apoptosis and tubular complex for mation was examined in caerulein-induced pancreatitis using histology, immu nohistochemistry, electron microscopy and DNA gel electrophoresis. Rats wer e given 8 hourly subcutaneous injections of caerulein, 24 mu g/kg, for up t o 2 days. Morphologically and biochemically typical apoptosis affected 4.6 and 8.9% of acinar cells at 1 and 2 days, respectively, resulting in remova l of most acinar cells by 2 days. Consequently, pancreatic ducts, the linin g cells expressing bcl-2 and therefore resistant to apoptosis, became much more closely approximated to form the basis of tubular complexes; small num bers of immunohistochemically discrete acinar cells in their lining were ei ther pre-apoptotic resistant to it or newly formed. Proliferation of duct-l ike lining cells was associated with apoptosis, an increase in islet cells and acinar cell regeneration. There was evidence of duct to acinar cell dif ferentiation but the main increase in acinar cell numbers appeared to deriv e from proliferation of newly formed acinar cells.