title: Hepatic transdifferentiation in the pancreas.
abstract: The differentiated state of specialized cells appears to be dependent on interactions between the extracellular microenvironment, cytoplasmic signals and DNA. Perturbations in these interactions lead to phenotypic alterations of the cell--referred to as transdifferentiation. Copper deficiency in rats leads to global acinar cell loss due to apoptosis possibly leading to perturbations in cell-cell interactions and the microenvironment. Acinar cell loss is associated with the proliferation of ductular epithelial and oval cells. Massive depletion of the acinar cell pool creates severe expansion pressure on oval and ductular cells to fill the vacuity. This probably causes a change in the commitment of these cells resulting in transdifferentiation into hepatocytes. Pancreatic hepatocytes exhibit all the morphological and functional properties of liver parenchymal cells.
authors.affiliation: Department of Pathology, Northwestern University Medical School, Chicago, IL 60611-3008, USA.
authors.forename: M S
authors.initials: MS
authors.lastname: Rao
authors.forename: J K
authors.initials: JK
authors.lastname: Reddy
mesh_terms: D000818:Animals; D017209:Apoptosis; D002454:Cell Differentiation; D003300:Copper / Q000172:deficiency*; D008099:Liver / Q000166:cytology; D010179:Pancreas / Q000473:pathology*; D051381:Rats
chemical_list: D003300:Copper