Document Detail


Expression of extracellular matrix genes in cultured hepatic oval cells: an origin of hepatic stellate cells through transforming growth factor beta?
MedLine Citation:
PMID:  19323784     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Hepatic oval cells, progenitor cells in the liver, can differentiate into hepatocytes and bile duct cells both in vitro and in vivo. Although hepatic stellate cells are another important cell component in the liver, less attention has been focused on the relationship between hepatic oval cells and hepatic stellate cells. METHODS: Hepatic oval cells were isolated from rats fed a choline-deficient diet supplemented with 0.1% ethionine for 6 weeks and characterized by electron microscopy, flow cytometry, reverse transcription polymerase chain reaction, Western blot and bi-direction differentiation. After treatment with transforming growth factor-beta1 (TGF-beta1), changes in cell viability, morphology, extracellular matrix (ECM) expression and immune phenotype were analysed in these cultured and adherent hepatic oval cells. RESULTS: The primary cultured hepatic oval cells were positive for the oval cell-specific markers OV-6, BD-1/BD-2 and M2PK as well as the hepatocyte markers albumin and alpha-foetoprotein. These hepatic oval cells differentiated bipotentially into hepatocytes or bile duct-like cells under appropriate conditions. It is noteworthy that these bipotential hepatic oval cells expressed ECM genes stably, including collagens, matrix metalloproteinases and tissue inhibitor of mellatoproteinase. Furthermore, except for growth inhibition and morphological changes in the hepatic oval cells after exposure to TGF-beta1, there was an increased expression of ECM genes, the onset expression of snail and loss expression of E-cadherin. During this process, TGF-beta1 treatment induced an upregulation of marker genes for hepatic stellate cells in hepatic oval cells, such as desmin and GFAP. CONCLUSION: Except for the expression of ECM, the cultured hepatic oval cells could induce an increased expression of hepatic stellate cell markers by TGF-beta1 through an epithelial-mesenchymal transition process, which might indicate the contribution of hepatic oval cells to liver fibrosis.
Authors:
Ping Wang; Tianhui Liu; Min Cong; Xiaoning Wu; Yanfeng Bai; Chenghong Yin; Wei An; Baoen Wang; Jidong Jia; Hong You
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Liver international : official journal of the International Association for the Study of the Liver     Volume:  29     ISSN:  1478-3231     ISO Abbreviation:  Liver Int.     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-03-27     Completed Date:  2009-06-25     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101160857     Medline TA:  Liver Int     Country:  England    
Other Details:
Languages:  eng     Pagination:  575-84     Citation Subset:  IM    
Affiliation:
Liver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
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MeSH Terms
Descriptor/Qualifier:
Albumins / metabolism
Animals
Antimetabolites / administration & dosage,  adverse effects
Bile Ducts / drug effects,  metabolism,  pathology
Biological Markers / metabolism
Cadherins / metabolism
Cell Differentiation / drug effects
Cell Survival / drug effects
Cells, Cultured
Choline Deficiency / etiology,  metabolism,  pathology
Desmin / genetics,  metabolism
Disease Models, Animal
Ethionine / administration & dosage,  adverse effects
Extracellular Matrix Proteins / drug effects,  genetics,  metabolism*,  pharmacology
Gene Expression / drug effects*
Glial Fibrillary Acidic Protein / genetics,  metabolism
Hepatocytes / drug effects,  metabolism,  pathology
Liver / metabolism*,  pathology
Male
RNA, Messenger / metabolism
Rats
Rats, Sprague-Dawley
Stem Cells / drug effects,  metabolism*,  ultrastructure
Transforming Growth Factor beta / metabolism*,  pharmacology
alpha-Fetoproteins / metabolism
Chemical
Reg. No./Substance:
0/Albumins; 0/Antimetabolites; 0/Biological Markers; 0/Cadherins; 0/Desmin; 0/Extracellular Matrix Proteins; 0/Glial Fibrillary Acidic Protein; 0/RNA, Messenger; 0/Transforming Growth Factor beta; 0/alpha-Fetoproteins; 13073-35-3/Ethionine; 148710-76-3/betaIG-H3 protein

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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