UMMS Affiliation

Program in Molecular Medicine; UMass Metabolic Network

Date

4-5-2016

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.

Rights and Permissions

Citation: 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

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/).

Related Resources

Link to Article in PubMed

Keywords

JNK, myeloid, inflammation, inflammatory cells, hepatitis, hepatocellular carcinoma

PubMed ID

27052181

Creative Commons License

Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

 
 

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