Ultrastructure of the rat pancreas after experimental duct ligation. I. The role of apoptosis and intraepithelial macrophages in acinar cell deletion.
After ligation of the rat pancreas, acinar cells disappeared from the distal gland within 5 days. Necrosis was responsible for minor cell loss during the first 24 hours, but most of the acinar cells were deleted by apoptosis. This distinctive form of cell death, which has been implicated in atrophy of other tissues, was characterized by cellular condensation followed by surface budding to produce membrane-bounded apoptotic bodies. Most of these were ingested and degraded by mononuclear phagocytes resident within the epithelium and a few by adjoining acinar cells. As atrophy progressed, the phagocytes increased in number through division and immigration of monocytes. The apoptotic deletion of acinar cells was characteristically effected without basement membrane disruption and was accompanied by simultaneous duct cell proliferation. The consequent rapid glandular remodeling resulted in reduction of the lobules to clusters of ductules in a collagenous stroma.
D000818:Animals; D002470:Cell Survival; D003251:Constriction, Pathologic; D004848:Epithelium / Q000473:pathology / Q000648:ultrastructure; D008026:Ligation; D008264:Macrophages / Q000473:pathology* / Q000648:ultrastructure; D008297:Male; D008854:Microscopy, Electron; D009336:Necrosis; D010179:Pancreas / Q000473:pathology / Q000648:ultrastructure*; D010183:Pancreatic Ducts / Q000473:pathology*; D051381:Rats; D011919:Rats, Inbred Strains