Program in Molecular Medicine; UMass Metabolic Network
Biochemistry | Cancer Biology | Cell Biology | Cellular and Molecular Physiology | Digestive System Diseases | Molecular Biology | Pathological Conditions, Signs and Symptoms
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.
JNK, myeloid, inflammation, inflammatory cells, hepatitis, hepatocellular carcinoma
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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
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
Han MS, Barrett T, Brehm MA, Davis RJ. (2016). Inflammation Mediated by JNK in Myeloid Cells Promotes the Development of Hepatitis and Hepatocellular Carcinoma. Davis Lab Publications. https://doi.org/10.1016/j.celrep.2016.03.008. Retrieved from https://escholarship.umassmed.edu/davis/88
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This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.
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