Publication: Proliferation and differentiation of
ductular progenitor cells and littoral cells during
the regeneration of the rat liver to CCl4/2-AAF injury
Loading...
Date
2002
Authors
Yin, L. ; Lynch, D. ; Ilic, Z. ; Sell, S.
item.page.secondaryauthor
item.page.director
Publisher
Murcia : F. Hernández
publication.page.editor
publication.page.department
DOI
item.page.type
info:eu-repo/semantics/article
Description
Abstract
Restoration of centrolobular injury induced
by carbon tetrachloride (CCl 4), when hepatocyte
proliferation is inhibited by treatment with N-2-
acetylaminofluorene (AAF), is accomplished by
proliferation of ductular progenitor cells, that arise
intraportally and extend into the liver lobule. This
pattern contrasts to the restitutive proliferation of
hepatocytes when AAF is not administered, and the
proliferation of non-ductular periportal oval cells follows
periportal necrosis induced by allyl alcohol. The
expanding ducts stain for alphafetoprotein (AFP), OV-6,
pan-cytokeratin (CKPan), and laminin. The neoductular
proliferation is accompanied by fibronectin-positive
K u p ffer cells and desmin-positive stellate (Ito) cells,
which may play critical roles not only in controlling
proliferation and differentiation of ductular progenitor
cells, but also in reestablishing hepatic cord structure.
When AAF is discontinued 7 days after injury, clusters
of small hepatocytes appear next to the neoductules.
Some of these small hepatocytes, as well as some larger
hepatocytes adjacent to the ducts, stain for AFP and for
carbamoylphosphate synthetase I (CPS-I), suggesting
that the ductular progenitor cells may differentiate into
hepatocytes when AAF is withdrawn. The restitutive
process is facilitated by clearing of the central necrotic
zone by infiltrating macrophages and co-migration of
mature hepatocytes, with Kupffer cells and stellate cells,
into the necrotic zone.
publication.page.subject
Citation
item.page.embargo
Ir a Estadísticas
Sin licencia Creative Commons.