ULTRASTRUCTURE OF THE RAT PANCREAS AFTER EXPERIMENTAL DUCT LIGATION .2. DUCT AND STROMAL CELL-PROLIFERATION, DIFFERENTIATION, AND DELETION

被引:75
作者
WALKER, NI
WINTERFORD, CM
KERR, JFR
机构
[1] Department of Pathology, Princess Alexandra Hospital, Woolloongabba
[2] Department of Pathology, University of Queensland Medical School, Herston, Brisbane, QLD
关键词
APOPTOSIS; ATROPHY; CELL PROLIFERATION; DIFFERENTIATION; DUCT LIGATION; PANCREAS; ULTRASTRUCTURE;
D O I
10.1097/00006676-199207000-00002
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Ligation of the pancreas in rats was followed by rapid atrophy of the distal part of the gland, where deletion of the acinar cells by apoptosis and simultaneous extensive proliferation of duct cells resulted in the lobules being converted into groups of closely packed small ducts within 5 days. We found no ultrastructural evidence that cells lining these small ducts arose from acinar cells by a process of dedifferentiation, as has been suggested by some investigators. During the succeeding weeks, some of the ductal lining cells developed islet cell or partial acinar cell differentiation. The latter soon died by apoptosis, and some ductlike and islet cells were also deleted by this means. Most of the apoptotic bodies formed in the ducts were phagocytosed by intraepithelial macrophages. In the longer term, continuing apoptosis eventually resulted in the disappearance of many ducts, only their thickened basal laminae remaining. Differentiation of stromal fibroblasts into contractile myofibroblasts may have contributed to shrinkage of the duct-obstructed glandular tissue, and apoptosis of endothelial cells probably accounted for the associated reduction of the capillary bed.
引用
收藏
页码:420 / 434
页数:15
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共 59 条
[1]  
Boquist L., Edstrom C., Ultrastructure of pancreatic acinar and islet parenchyma in rats at various intervals after duct ligation, Virchows Arch [A], 349, pp. 69-79, (1970)
[2]  
Churg A., Richter W.R., Early changes in the exocrine pancreas of the dog and rat after ligation of the pancreatic duct: A light and electron microscopic study, Am J Pathol, 63, pp. 521-534, (1971)
[3]  
Zeligs J.D., Janoff A., Dumont A.E., The course and nature of acinar cell death following pancreatic ligation in the guinea pig, Am J Pathol, 80, pp. 203-226, (1975)
[4]  
Pound A.W., Walker N.I., Involution of the pancreas after ligation of the pancreatic ducts. I. A histological study, Br J Exp Pathol, 62, pp. 547-558, (1981)
[5]  
Graves A.J., Holmquist D., Githens S., Effect of duct obstruction on histology and on activities of 7-glutamyl transferase, adenosine triphosphatase, alkaline phosphatase, and amylase in rat pancreas, Dig Dis Sci, 31, pp. 1254-1264, (1986)
[6]  
Githens S., The pancreatic duct cell: Proliferative capabilities, specific characteristics, metaplasia, isolation, and culture, J Pediatr Gastroenterol Nutr, 7, pp. 486-506, (1988)
[7]  
Bockman D.E., Cells of origin of pancreatic cancer: Experimental animal tumors related to human pancreas, Cancer, 47, pp. 1528-1534, (1981)
[8]  
Bockman D.E., Black O., Mills L.R., Webster P.D., Origin of tubular complexes developing during induction of pancreatic adenocarcinoma by 7,12-dimethylbenz(A)anthracene, Am J Pathol, 90, pp. 645-658, (1978)
[9]  
Rao M.S., Reddy J.K., Histogenesis of pseudo-ductular changes induced in the pancreas of guinea pigs treated with N-methyl-Af-nitrosourea, Carcinogenesis, 1, pp. 1027-1037, (1980)
[10]  
Flaks B., Moore M.A., Flaks A., Ultrastructural analysis of pancreatic carcinogenesis. IV. Pseudoductular transformation of acini in the hamster pancreas during 7V-nitroso-bis(2-hydroxypropyl)amine carcinogenesis, Carcinogenesis, 2, pp. 1241-1253, (1981)