help button home button Am J Pathol Epitomics, Inc.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Braun, K. M.
Right arrow Articles by Sandgren, E. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Braun, K. M.
Right arrow Articles by Sandgren, E. P.
(American Journal of Pathology. 2000;157:561-569.)
© 2000 American Society for Investigative Pathology

Regular Articles

Cellular Origin of Regenerating Parenchyma in a Mouse Model of Severe Hepatic Injury

Kristin M. Braun and Eric P. Sandgren

From the Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, Wisconsin

Several treatments in rodents, including administration of the alkylating agent dipin, followed by two-thirds partial hepatectomy in mice combine destruction of liver parenchyma with hepatocyte mitoinhibition. These treatments induce proliferation of bile epithelial-like cells (termed oval cells), development of foci composed of small hepatocytes, and eventual replacement of damaged parenchyma by healthy hepatocytes. It has been proposed that these oval cells represent transitional cells in a nonhepatocytic liver facultative stem cell lineage that can give rise to the small hepatocyte foci, and that these foci eventually become confluent and replace liver parenchyma. In this study, we used in vivo cell lineage marking in genetically chimeric livers to test the hypothesis that hepatocytes can serve as the precursor cell type to the small hepatocyte foci that develop in mouse liver after treatment with dipin plus partial hepatectomy. Although we do not exclude the possibility that some small hepatocyte foci may be stem cell-derived, we demonstrate that hepatocyte-derived foci are present after dipin-induced liver damage in mice.




This article has been cited by other articles:


Home page
 Exp Biol MedHome page
M. A. Suckow, A. Zollman, I. Cornelissen, M. Casad, J. Roahrig, F. J. Castellino, and E. D. Rosen
Tissue Distribution of Fetal Liver Cells Following In Utero Transplantation in Mice
Exp Biol Med, December 1, 2005; 230(11): 860 - 864.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
K. M. Braun, A. W. Thompson, and E. P. Sandgren
Hepatic Microenvironment Affects Oval Cell Localization in Albumin-Urokinase-Type Plasminogen Activator Transgenic Mice
Am. J. Pathol., January 1, 2003; 162(1): 195 - 202.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
T. C. Weglarz, J. L. Degen, and E. P. Sandgren
Hepatocyte Transplantation into Diseased Mouse Liver : Kinetics of Parenchymal Repopulation and Identification of the Proliferative Capacity of Tetraploid and Octaploid Hepatocytes
Am. J. Pathol., December 1, 2000; 157(6): 1963 - 1974.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2000 by the American Society for Investigative Pathology.