help button home button Am J Pathol R & D Systems
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 Sekhon, S. S.
Right arrow Articles by Monga, S. P.S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sekhon, S. S.
Right arrow Articles by Monga, S. P.S.
(American Journal of Pathology. 2004;164:2229-2240.)
© 2004 American Society for Investigative Pathology

Fibroblast Growth Factor Enriches the Embryonic Liver Cultures for Hepatic Progenitors

Sandeep S. Sekhon*, Xinping Tan{dagger}, Amanda Micsenyi{dagger}, William C. Bowen{dagger} and Satdarshan P.S. Monga{dagger}

From the Department of Internal Medicine,*Allegheny General Hospital, Pittsburgh; and the Department of Pathology,{dagger}University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania

Fibroblast growth factors (FGFs) play an important role in hepatic induction during development. The aim of our study was to investigate the effect of exogenous FGFs on ex vivo liver development. We begin our analysis by examining FGF signaling during early mouse liver development. Phospho-FGF receptor (Tyr653/654) was detected in embryonic day 10 (E10) to E12 livers only. Next, E10 livers were cultured in the presence of FGF1, FGF4, or FGF8 for 72 hours and examined for histology, proliferation, apoptosis, and differentiation. FGFs especially FGF8 promoted sheet-like architecture, cell proliferation, and survival as compared to the control. All FGFs induced a striking increase in the number of c-kit and {alpha}-fetoprotein-positive progenitors, without altering albumin staining. However these progenitors were CK-19-positive (biliary and bipotential progenitor marker) only in the presence of FGF1 or FGF4 and not FGF8. FGFs also induced ß-catenin, a stem cell renewal factor in these cultures. In conclusion, the presence of activated FGFR indicates a physiological role of FGF during early liver development. FGF1 and FGF4 enrich the embryonic liver cultures for bipotential hepatic progenitors. FGF8 promotes such enrichment and induces a one-step differentiation toward a unipotential hepatocyte progenitor. Thus, FGFs might be useful for enrichment and propagation of developmental hepatic progenitors.




This article has been cited by other articles:


Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
U. Apte, G. Zeng, M. D. Thompson, P. Muller, A. Micsenyi, B. Cieply, K. H. Kaestner, and S. P. S. Monga
beta-Catenin is critical for early postnatal liver growth
Am J Physiol Gastrointest Liver Physiol, June 1, 2007; 292(6): G1578 - G1585.
[Abstract] [Full Text] [PDF]

Home page
 Stem CellsHome page
M. H. Walkup and D. A. Gerber
Hepatic Stem Cells: In Search of
Stem Cells, August 1, 2006; 24(8): 1833 - 1840.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
S. P.S. Monga, M. S. Hout, M. J. Baun, A. Micsenyi, P. Muller, L. Tummalapalli, A. R. Ranade, J.-H. Luo, S. C. Strom, and J. C. Gerlach
Mouse Fetal Liver Cells in Artificial Capillary Beds in Three-Dimensional Four-Compartment Bioreactors
Am. J. Pathol., November 1, 2005; 167(5): 1279 - 1292.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2004 by the American Society for Investigative Pathology.