UMMS Affiliation
Program in Molecular Medicine; UMass Metabolic Network
Publication Date
2016-04-05
Document Type
Article
Disciplines
Biochemistry | Cancer Biology | Cell Biology | Cellular and Molecular Physiology | Digestive System Diseases | Molecular Biology | Pathological Conditions, Signs and Symptoms
Abstract
The cJun NH2-terminal kinase (JNK) signaling pathway is required for the development of hepatitis and hepatocellular carcinoma. A role for JNK in liver parenchymal cells has been proposed, but more recent studies have implicated non-parenchymal liver cells as the relevant site of JNK signaling. Here, we tested the hypothesis that myeloid cells mediate this function of JNK. We show that mice with myeloid cell-specific JNK deficiency exhibit reduced hepatic inflammation and suppression of both hepatitis and hepatocellular carcinoma. These data identify myeloid cells as a site of pro-inflammatory signaling by JNK that can promote liver pathology. Targeting myeloid cells with a drug that inhibits JNK may therefore provide therapeutic benefit for the treatment of inflammation-related liver disease.
Keywords
JNK, myeloid, inflammation, inflammatory cells, hepatitis, hepatocellular carcinoma
Rights and Permissions
Copyright 2016 The Authors. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
DOI of Published Version
10.1016/j.celrep.2016.03.008
Source
Cell Rep. 2016 Apr 5;15(1):19-26. doi: 10.1016/j.celrep.2016.03.008. Epub 2016 Mar 24. Link to article on publisher's site
Journal/Book/Conference Title
Cell reports
Related Resources
PubMed ID
27052181
Repository Citation
Han, Myoung Souk; Barrett, Tamera; Brehm, Michael A.; and Davis, Roger J., "Inflammation Mediated by JNK in Myeloid Cells Promotes the Development of Hepatitis and Hepatocellular Carcinoma" (2016). Davis Lab Publications. 88.
https://escholarship.umassmed.edu/davis/88
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.
Included in
Biochemistry Commons, Cancer Biology Commons, Cell Biology Commons, Cellular and Molecular Physiology Commons, Digestive System Diseases Commons, Molecular Biology Commons, Pathological Conditions, Signs and Symptoms Commons