ACLS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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 Google Scholar
Google Scholar
Right arrow Articles by Parkes, J. G.
Right arrow Articles by Templeton, D. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Parkes, J. G.
Right arrow Articles by Templeton, D. M.
Annals of Clinical & Laboratory Science 33:295-305 (2003)
© 2003 Association of Clinical Scientists

Effects of Retinol and Hepatocyte-Conditioned Medium on Cultured Rat Hepatic Stellate Cells

Joel G. Parkes and Douglas M. Templeton
Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada

Address correspondence to Douglas M. Templeton, M.D., Ph.D., Dept. of Laboratory Medicine and Pathobiology, University of Toronto, 1 King’s College Circle, Toronto, Ontario M5S 1A8, Canada; tel 416 978 3972; fax 416 978 5959, e-mail doug.templeton{at}utoronto.ca.

Hepatic stellate cells (HSC) become activated in liver injury, proliferating and secreting components of connective tissue. Activated HSC lose their native retinol and fat storing capacity. Signals from hepatocytes and/or Kupffer cells injured (eg, by iron overload) may contribute to the so-called activated HSC phenotype. Primary rat HSC cultures were treated with retinol to determine if this could produce a quiescent cell for controlled in vitro studies of activation. Retinol resulted in suppressed DNA synthesis in proliferating HSC, a reorganization of actin filaments, and a return of fat storage. However, it did not suppress the expression of fibrogenic genes such as those for collagens type I and IV, and TGF-ß1. Furthermore, retinol-treated cells may increase expression of these genes in response to conditioned medium from hepatocyte cultures. The effect is especially apparent for collagen type I mRNA, and with conditioned medium from iron-loaded hepatocytes. Thus, retinol may be a two-edged sword in iron overload, potentially suppressing HSC proliferation on the one hand, and sensitizing a fibrogenic pattern of gene expression on the other. Factors influencing this balance merit further study.

Keywords: hepatic stellate cell, hepatocyte, Kupffer cell, fibrosis, iron overload, {alpha}-actin, collagen






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2003 by the Association of Clinical Scientists.