Informacja

Drogi użytkowniku, aplikacja do prawidłowego działania wymaga obsługi JavaScript. Proszę włącz obsługę JavaScript w Twojej przeglądarce.

Tytuł pozycji:

β-Catenin and interleukin-1β-dependent chemokine (C-X-C motif) ligand 10 production drives progression of disease in a mouse model of congenital hepatic fibrosis.

Tytuł:
β-Catenin and interleukin-1β-dependent chemokine (C-X-C motif) ligand 10 production drives progression of disease in a mouse model of congenital hepatic fibrosis.
Autorzy:
Kaffe E; Section of Digestive Diseases, Liver Center, Yale University, New Haven, CT.
Fiorotto R; Section of Digestive Diseases, Liver Center, Yale University, New Haven, CT.; International Center for Digestive Health, University of Milan-Bicocca, Milan, Italy.
Pellegrino F; Section of Digestive Diseases, Liver Center, Yale University, New Haven, CT.
Mariotti V; Section of Digestive Diseases, Liver Center, Yale University, New Haven, CT.; International Center for Digestive Health, University of Milan-Bicocca, Milan, Italy.; Department of Molecular Medicine, University of Padua, School of Medicine, Padua, Italy.
Amenduni M; Section of Digestive Diseases, Liver Center, Yale University, New Haven, CT.
Cadamuro M; International Center for Digestive Health, University of Milan-Bicocca, Milan, Italy.
Fabris L; International Center for Digestive Health, University of Milan-Bicocca, Milan, Italy.; Department of Molecular Medicine, University of Padua, School of Medicine, Padua, Italy.
Strazzabosco M; Section of Digestive Diseases, Liver Center, Yale University, New Haven, CT.; International Center for Digestive Health, University of Milan-Bicocca, Milan, Italy.
Spirli C; Section of Digestive Diseases, Liver Center, Yale University, New Haven, CT.; International Center for Digestive Health, University of Milan-Bicocca, Milan, Italy.
Źródło:
Hepatology (Baltimore, Md.) [Hepatology] 2018 May; Vol. 67 (5), pp. 1903-1919. Date of Electronic Publication: 2018 Mar 25.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural
Język:
English
Imprint Name(s):
Publication: 2023- : [Philadelphia] : Wolters Kluwer Health, Inc.
Original Publication: Baltimore, MD : Williams & Wilkins, [c1981]-
MeSH Terms:
Chemokine CXCL10/*metabolism
Genetic Diseases, Inborn/*metabolism
Interleukin-1beta/*metabolism
Liver Cirrhosis/*metabolism
beta Catenin/*metabolism
Animals ; Blotting, Western ; Disease Models, Animal ; Disease Progression ; Epithelial Cells/metabolism ; Flow Cytometry ; Immunohistochemistry ; Liver/metabolism ; Liver/pathology ; Mice ; Real-Time Polymerase Chain Reaction ; Receptors, CXCR3/metabolism ; Signal Transduction
References:
Gastroenterology. 2011 Jun;140(7):1855-9, 1859.e1. (PMID: 21515270)
Trends Immunol. 2011 Mar;32(3):110-6. (PMID: 21333600)
J Clin Invest. 2012 Feb;122(2):586-99. (PMID: 22251704)
Gastroenterology. 2010 Jan;138(1):360-371.e7. (PMID: 19766642)
J Biol Chem. 2004 Dec 31;279(53):55633-43. (PMID: 15489227)
Am J Pathol. 2008 Feb;172(2):417-29. (PMID: 18202188)
J Biol Chem. 2010 Sep 17;285(38):29101-10. (PMID: 20833730)
J Gastroenterol Hepatol. 2000 Mar;15(3):244-53. (PMID: 10764023)
Cell. 2014 May 22;157(5):1013-22. (PMID: 24855941)
J Hepatol. 2012 Sep;57(3):642-54. (PMID: 22634126)
J Biol Chem. 2010 Aug 6;285(32):24793-804. (PMID: 20516073)
PLoS One. 2013 Jul 29;8(7):e69585. (PMID: 23922745)
J Immunol. 2013 Jul 1;191(1):323-36. (PMID: 23740952)
Cancer Res. 2006 Aug 1;66(15):7701-7. (PMID: 16885372)
Int J Colorectal Dis. 2008 Mar;23(3):305-17. (PMID: 18046562)
J Clin Invest. 2002 May;109(9):1143-8. (PMID: 11994402)
J Hepatol. 2014 Dec;61(6):1365-75. (PMID: 25048951)
PLoS One. 2016 Mar 03;11(3):e0150606. (PMID: 26938654)
Hepatology. 2013 Nov;58(5):1713-23. (PMID: 23744610)
PLoS One. 2015 Dec 23;10(12):e0145342. (PMID: 26699615)
J Hepatol. 2012 May;56(5):1159-70. (PMID: 22245898)
J Autoimmun. 2010 Dec;35(4):424-35. (PMID: 20932719)
Genes Dev. 2007 Jun 1;21(11):1396-408. (PMID: 17510282)
Semin Liver Dis. 2011 Feb;31(1):11-32. (PMID: 21344348)
Int J Mol Med. 2014 Aug;34(2):632-8. (PMID: 24938929)
J Clin Gastroenterol. 2005 Apr;39(4 Suppl 2):S90-S102. (PMID: 15758666)
Gastroenterology. 2012 Nov;143(5):1158-72. (PMID: 22982943)
J Neurovirol. 1999 Feb;5(1):82-94. (PMID: 10190694)
J Clin Invest. 2012 Oct;122(10 ):3476-89. (PMID: 22945633)
Hepatology. 2015 Dec;62(6):1828-39. (PMID: 26313562)
Mol Cell Biol. 2005 Sep;25(18):7966-75. (PMID: 16135789)
Cell. 2010 Mar 19;140(6):821-32. (PMID: 20303873)
Cell Mol Immunol. 2016 May;13(3):316-27. (PMID: 26908374)
Gastroenterology. 2014 Sep;147(3):577-594.e1. (PMID: 25066692)
Annu Rev Immunol. 2009;27:519-50. (PMID: 19302047)
J Hepatol. 2017 Mar;66(3):571-580. (PMID: 27826057)
J Immunol. 2009 Oct 15;183(8):5129-37. (PMID: 19783677)
Hepatology. 2016 Mar;63(3):965-82. (PMID: 26645994)
Gastroenterology. 2004 Nov;127(5):1565-77. (PMID: 15521023)
J Cell Sci. 2008 Jul 1;121(Pt 13):2224-34. (PMID: 18565826)
Annu Rev Med. 2009;60:321-37. (PMID: 18947299)
Science. 2000 Oct 6;290(5489):144-7. (PMID: 11021801)
Hepatology. 2016 Dec;64(6):2118-2134. (PMID: 27629435)
Sci Rep. 2016 Jun 28;6:28786. (PMID: 27349927)
Biochem J. 2002 Oct 1;367(Pt 1):97-105. (PMID: 12057007)
Annu Rev Immunol. 2015;33:823-74. (PMID: 25706096)
Nat Rev Immunol. 2013 Jun;13(6):397-411. (PMID: 23702978)
Grant Information:
P30 DK034989 United States DK NIDDK NIH HHS; R01 DK079005 United States DK NIDDK NIH HHS; R01 DK101528 United States DK NIDDK NIH HHS
Substance Nomenclature:
0 (Chemokine CXCL10)
0 (Interleukin-1beta)
0 (Receptors, CXCR3)
0 (beta Catenin)
SCR Disease Name:
Hepatic Fibrosis, Congenital
Entry Date(s):
Date Created: 20171116 Date Completed: 20181024 Latest Revision: 20190610
Update Code:
20240105
PubMed Central ID:
PMC5906178
DOI:
10.1002/hep.29652
PMID:
29140564
Czasopismo naukowe
Congenital hepatic fibrosis (CHF), a genetic disease caused by mutations in the polycystic kidney and hepatic disease 1 (PKHD1) gene, encoding for the protein fibrocystin/polyductin complex, is characterized by biliary dysgenesis, progressive portal fibrosis, and a protein kinase A-mediated activating phosphorylation of β-catenin at Ser675. Biliary structures of Pkhd1 del4/del4 mice, a mouse model of CHF, secrete chemokine (C-X-C motif) ligand 10 (CXCL10), a chemokine able to recruit macrophages. The aim of this study was to clarify whether CXCL10 plays a pathogenetic role in disease progression in CHF/Caroli disease and to understand the mechanisms leading to increased CXCL10 secretion. We demonstrate that treatment of Pkhd1 del4/del4 mice for 3 months with AMG-487, an inhibitor of CXC chemokine receptor family 3, the cognate receptor of CXCL10, reduces the peribiliary recruitment of alternative activated macrophages (cluster of differentiation 45 + F4/80 + cells), spleen size, liver fibrosis (sirius red), and cyst growth (cytokeratin 19-positive area), consistent with a pathogenetic role of CXCL10. Furthermore, we show that in fibrocystin/polyductin complex-defective cholangiocytes, isolated from Pkhd1 del4/del4 mice, CXCL10 production is mediated by Janus kinase/signal transducer and activator of transcription 3 in response to interleukin 1beta (IL-1β) and β-catenin. Specifically, IL-1β promotes signal transducer and activator of transcription 3 phosphorylation, whereas β-catenin promotes its nuclear translocation. Increased pro-IL-1β was regulated by nuclear factor kappa-light-chain-enhancer of activated B cells, and increased secretion of active IL-1β was mediated by the activation of Nod-like receptors, pyrin domain containing 3 inflammasome (increased expression of caspase 1 and Nod-like receptors, pyrin domain containing 3).
Conclusion: In fibrocystin/polyductin complex-defective cholangiocytes, β-catenin and IL-1β are responsible for signal transducer and activator of transcription 3-dependent secretion of CXCL10; in vivo experiments show that the CXCL10/CXC chemokine receptor family 3 axis prevents the recruitment of macrophages, reduces inflammation, and halts the progression of the disease; the increased production of IL-1β highlights the autoinflammatory nature of CHF and may open novel therapeutic avenues. (Hepatology 2018;67:1903-1919).
(© 2017 by the American Association for the Study of Liver Diseases.)

Ta witryna wykorzystuje pliki cookies do przechowywania informacji na Twoim komputerze. Pliki cookies stosujemy w celu świadczenia usług na najwyższym poziomie, w tym w sposób dostosowany do indywidualnych potrzeb. Korzystanie z witryny bez zmiany ustawień dotyczących cookies oznacza, że będą one zamieszczane w Twoim komputerze. W każdym momencie możesz dokonać zmiany ustawień dotyczących cookies