Immunohistochemical Evidence for Myofibroblast-like Cells Associated with Liver Injury Induced by Aflatoxin B1 in Rainbow Trout (Oncorhynchus mykiss)

In mammalian species, profibrogenic cells are activated to become myofibroblasts in response to liver damage. Few studies have examined hepatic myofibroblasts and their role in liver damage in teleosts. The aim of the present study was to investigate the involvement of myofibroblast-like cells in ra...

Full description

Saved in:
Bibliographic Details
Published in:Journal of comparative pathology Vol. 150; no. 2-3; pp. 258 - 265
Main Authors: Arana, S., Alves, V.A.F., Sabino, M., Tabata, Y.A., Nonogaki, S., Zaidan-Dagli, M.-L., Hernandez-Blazquez, F.J.
Format: Journal Article
Language:English
Published: England Elsevier Ltd 01-02-2014
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:In mammalian species, profibrogenic cells are activated to become myofibroblasts in response to liver damage. Few studies have examined hepatic myofibroblasts and their role in liver damage in teleosts. The aim of the present study was to investigate the involvement of myofibroblast-like cells in rainbow trout (Oncorhynchus mykiss) with hepatic damage induced by aflatoxin B1 (AFB1). Histopathological and immunohistochemical analyses characterized alterations in the liver stroma during the carcinogenic process. Anti-human α-smooth muscle actin (SMA) and anti-human desmin primary antibodies were used in immunohistochemistry. Only the anti-SMA reagent labelled cells in trout liver. In the livers of control fish, only smooth muscle in blood vessels and around bile ducts was labelled. In the livers from AFB1-treated fish, SMA-positive cells were present in the stroma surrounding neoplastic lesions and in areas of desmoplastic reaction. These observations indicate that in teleosts, as in mammals, the myofibroblast-like cell is involved in fibrosis associated with liver injury. Chronic liver injury induced in trout by aflatoxin may provide a useful model system for study of the evolution of such mechanisms.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0021-9975
1532-3129
DOI:10.1016/j.jcpa.2013.07.003