| First Author | Han MS | Year | 2016 |
| Journal | Cell Rep | Volume | 15 |
| Issue | 1 | Pages | 19-26 |
| PubMed ID | 27052181 | Mgi Jnum | J:235078 |
| Mgi Id | MGI:5792758 | Doi | 10.1016/j.celrep.2016.03.008 |
| Citation | Han MS, et al. (2016) Inflammation Mediated by JNK in Myeloid Cells Promotes the Development of Hepatitis and Hepatocellular Carcinoma. Cell Rep 15(1):19-26 |
| abstractText | 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. |
