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
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.