HBV induces different responses of the hepatocytes and oval cells during HBV-related hepatic cirrhosis.
Animals
Apoptosis
Cell Proliferation
Cross-Sectional Studies
Disease Models, Animal
Gene Expression Profiling
/ methods
Gene Regulatory Networks
Hepatitis B
/ genetics
Hepatitis B virus
/ pathogenicity
Hepatocytes
/ cytology
Humans
Liver Cirrhosis
/ genetics
Mice
Mice, Transgenic
Oligonucleotide Array Sequence Analysis
Hepatic cirrhosis
Hepatitis B virus
Hepatocytes
Microarray
Oval cells
Journal
Cancer letters
ISSN: 1872-7980
Titre abrégé: Cancer Lett
Pays: Ireland
ID NLM: 7600053
Informations de publication
Date de publication:
28 02 2019
28 02 2019
Historique:
received:
05
10
2018
revised:
20
11
2018
accepted:
24
11
2018
pubmed:
7
12
2018
medline:
9
11
2019
entrez:
4
12
2018
Statut:
ppublish
Résumé
Although hepatitis B virus (HBV)-related cirrhosis and hepatocellular carcinoma (HCC) cause a sever health problem worldwide, the underlying mechanisms are still elusive. This study aimed to investigate the responses of different cell types isolated from HBV transgenic mice. A cross-sectional set of hepatocytes and oval cells were obtained from HBV transgenic and control mice. Flow cytometry, immunohistochemistry and microarray were applied to investigate the cell biology of the hepatocytes and oval cells. Our results showed that HBV induced the proliferation of both cell oval cells and hepatocytes, and induced cell death of HBV hepatocytes while had minimal effects on oval cells. Further molecular and pathways analysis identified some genes and signaling pathways may be responsible for the different responses between oval cells and hepatocytes. In addition, analyses of selectively ten genes by IHC staining in human samples were consistent with microarray data. In summary, HBV transgenic mice is a useful model for studying the biological behaviors of oval cells affected by HBV and HBV-cirrhosis. Also, our results help better understand the mechanisms of HBV induced cirrhosis, and provide novel progenitor markers or prognostic/therapeutic markers.
Identifiants
pubmed: 30503551
pii: S0304-3835(18)30686-4
doi: 10.1016/j.canlet.2018.11.020
pii:
doi:
Types de publication
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
47-55Informations de copyright
Copyright © 2018 Elsevier B.V. All rights reserved.