Impact of osteopontin on the development of non-alcoholic liver disease and related hepatocellular carcinoma.
acute-on-chronic liver failure
fibrosis
lipoapoptosis
metabolic syndrome
non-alcoholic fatty liver
Journal
Liver international : official journal of the International Association for the Study of the Liver
ISSN: 1478-3231
Titre abrégé: Liver Int
Pays: United States
ID NLM: 101160857
Informations de publication
Date de publication:
07 2020
07 2020
Historique:
received:
15
10
2019
revised:
14
02
2020
accepted:
31
03
2020
pubmed:
14
4
2020
medline:
22
6
2021
entrez:
14
4
2020
Statut:
ppublish
Résumé
Osteopontin, a multifunctional protein and inflammatory cytokine, is overexpressed in adipose tissue and liver in obesity and contributes to the induction of adipose tissue inflammation and non-alcoholic fatty liver (NAFL). Studies performed in both mice and humans also point to a potential role for OPN in malignant transformation and tumour growth. To fully understand the role of OPN on the development of NAFL-derived hepatocellular carcinoma (HCC), we applied a non-alcoholic steatohepatitis (NASH)-HCC mouse model on osteopontin-deficient (Spp1 Two-day-old wild-type and Spp1 Spp1 Lack of osteopontin dissociates NASH-fibrosis severity from overall survival and HCC malignant transformation in NAFLD, and is therefore a putative therapeutic target only for advanced chronic liver disease.
Sections du résumé
BACKGROUND & AIMS
Osteopontin, a multifunctional protein and inflammatory cytokine, is overexpressed in adipose tissue and liver in obesity and contributes to the induction of adipose tissue inflammation and non-alcoholic fatty liver (NAFL). Studies performed in both mice and humans also point to a potential role for OPN in malignant transformation and tumour growth. To fully understand the role of OPN on the development of NAFL-derived hepatocellular carcinoma (HCC), we applied a non-alcoholic steatohepatitis (NASH)-HCC mouse model on osteopontin-deficient (Spp1
METHODS
Two-day-old wild-type and Spp1
RESULTS
Spp1
CONCLUSIONS
Lack of osteopontin dissociates NASH-fibrosis severity from overall survival and HCC malignant transformation in NAFLD, and is therefore a putative therapeutic target only for advanced chronic liver disease.
Identifiants
pubmed: 32281248
doi: 10.1111/liv.14464
pmc: PMC7384114
doi:
Substances chimiques
Osteopontin
106441-73-0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1620-1633Informations de copyright
© 2020 The Authors. Liver International published by John Wiley & Sons Ltd.
Références
Mol Cell Biochem. 2002 Oct;239(1-2):193-7
pubmed: 12479585
Hepatol Commun. 2018 Sep 21;2(11):1344-1355
pubmed: 30411081
Nat Med. 2003 Apr;9(4):416-23
pubmed: 12640447
World J Diabetes. 2013 Jun 15;4(3):51-63
pubmed: 23772273
J Biol Chem. 1957 May;226(1):497-509
pubmed: 13428781
J Gastroenterol. 2000;35(9):696-701
pubmed: 11023041
Sci Rep. 2017 Nov 7;7(1):14655
pubmed: 29116108
Cell Death Dis. 2018 Mar 2;9(3):356
pubmed: 29500465
Cells. 2019 Mar 22;8(3):
pubmed: 30909521
Endocrinology. 2016 Feb;157(2):570-85
pubmed: 26650570
Diabetes. 2017 Aug;66(8):2241-2253
pubmed: 28490610
J Hepatol. 2015 Apr;62(1 Suppl):S131-43
pubmed: 25920082
Clin Chim Acta. 2010 May 2;411(9-10):675-8
pubmed: 20138033
Diabetes. 2009 Jan;58(1):125-33
pubmed: 18952835
Hepatology. 2015 May;61(5):1547-54
pubmed: 25125077
Histopathology. 2020 Jan;76(2):182-188
pubmed: 31433515
Diabetes. 2010 Apr;59(4):935-46
pubmed: 20107108
Proc Natl Acad Sci U S A. 2011 Sep 27;108(39):16381-5
pubmed: 21930939
J Hepatol. 2017 Dec;67(6):1134-1136
pubmed: 28966125
Diabetologia. 2011 Aug;54(8):2132-42
pubmed: 21562757
Proc Natl Acad Sci U S A. 1994 Nov 8;91(23):10878-82
pubmed: 7971976
World J Hepatol. 2015 Aug 18;7(17):2080-90
pubmed: 26301050
Nat Clin Pract Endocrinol Metab. 2006 Jun;2(6):335-48
pubmed: 16932311
Int J Cancer. 2011 May 15;128(10):2436-43
pubmed: 21128245
Am J Physiol Gastrointest Liver Physiol. 2004 Jul;287(1):G264-73
pubmed: 15044174
Biochem Biophys Res Commun. 1999 Mar 24;256(3):527-31
pubmed: 10080931
Hepatology. 2010 Aug;52(2):774-88
pubmed: 20683968
Gastroenterology. 2015 Aug;149(2):389-97.e10
pubmed: 25935633
Int J Biol Sci. 2016 Aug 06;12(9):1121-8
pubmed: 27570486
Anticancer Res. 2014 Sep;34(9):4849-55
pubmed: 25202066
Cell Cycle. 2014;13(9):1400-12
pubmed: 24626186
Liver Int. 2010 Jul;30(6):850-9
pubmed: 20408954
Liver Int. 2020 Jul;40(7):1620-1633
pubmed: 32281248
Gut. 2014 Nov;63(11):1805-18
pubmed: 24496779
Curr Opin Cell Biol. 2005 Apr;17(2):216-22
pubmed: 15780600
Cancer Lett. 2010 Dec 28;299(2):130-6
pubmed: 20826049
Gut. 2009 Apr;58(4):586-93
pubmed: 19017686
J Biol Chem. 2013 Dec 27;288(52):36994-7009
pubmed: 24240095
Endocrinology. 2003 Sep;144(9):4154-63
pubmed: 12933690
Proc Natl Acad Sci U S A. 2015 Jan 27;112(4):1143-8
pubmed: 25564660
Hepatology. 2012 May;55(5):1389-97
pubmed: 22183689
Biochim Biophys Acta. 2016 Jan;1862(1):135-44
pubmed: 26529285
Semin Liver Dis. 2010 Nov;30(4):402-10
pubmed: 20960379
Gastroenterology. 2007 Jun;132(7):2557-76
pubmed: 17570226
J Leukoc Biol. 2007 Jun;81(6):1504-11
pubmed: 17369493
Hepatology. 2006 Oct;44(4):865-73
pubmed: 17006923
Mediators Inflamm. 2017;2017:4049098
pubmed: 28769537
PLoS One. 2014 Jan 31;9(1):e87464
pubmed: 24498111
J Clin Invest. 2007 Oct;117(10):2877-88
pubmed: 17823662
Hepatology. 2012 Feb;55(2):483-90
pubmed: 21953299
Hepatology. 2011 Jun;53(6):1874-82
pubmed: 21360720
Gastroenterology. 2003 Aug;125(2):437-43
pubmed: 12891546
Med Mol Morphol. 2013 Sep;46(3):141-52
pubmed: 23430399
Hepatology. 2012 Jun;55(6):1965-75
pubmed: 22223197
Kidney Int. 2010 Apr;77(7):588-600
pubmed: 20130530
Endocrinology. 2008 Mar;149(3):1350-7
pubmed: 18048491
PLoS One. 2014 May 28;9(5):e98398
pubmed: 24871103