Publication: Liver growth factor antifibrotic activity in vivo is associated with a decrease in activation of hepatic stellate cells
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Date
2009
Authors
Díaz-Gil, Juan J. ; García-Monzón, Carmelo ; Rúa, Carmen ; Martín Sanz, Paloma ; Cereceda, Rosa M. ; Miquilena-Colina, María E. ; Machín, Celia ; Fernández Martínez, Amalia ; García Cañero, Rafael
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The antifibrotic activity of Liver Growth
Factor (LGF), a liver mitogen, was previously
demonstrated in several models of rat liver fibrosis and
even in extrahepatic sites, such as carotid artery in
hypertensive rats and rat CdCl2-induced lung fibrosis. In
the present study, we have attempted to examine in depth
its mechanism of antifibrotic action in bile duct-ligated
(BDL) rats, with special emphasis on its activity in
fibrogenic liver cells.
BDL rats received either LGF 9 μg/week for 2 or 3
weeks (BDL+LGF, n=20/group) or saline (BDL+S,
n=20/group), at times 0, week 2, or week 5 after
operation. Groups were compared in terms of liver a-
smooth muscle actin (SMA) content (western blotting
and immunohistochemistry), hepatic apoptosis, liver
desmin content (western blotting), and serum
endothelin-1 (ELISA).
LGF produced a marked decrease in liver a-SMA
content compared with saline-injected rats, especially
evident at longer times (5w and 8w; p<0.05),
accompanied by a decrease in hepatic a-SMA+ cells. This decrease was not due to the killing of activated
hepatic stellate cells (HSC) or myofibroblasts by LGF,
since there was a slight decrease in hepatic apoptosis
that was more evident at 2w (p<0.05). Moreover, LGF
did not seem to influence HSC proliferation, as shown
by measuring liver desmin content. The antifibrotic
activity exerted by LGF seems to be closely related to a
modulation of the activation state of fibrogenic liver
cells (activated HSC and myofibroblasts) in BDL rats.
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