| First Author | Bourdi M | Year | 2008 |
| Journal | Biochem Biophys Res Commun | Volume | 374 |
| Issue | 1 | Pages | 6-10 |
| PubMed ID | 18586006 | Mgi Jnum | J:139164 |
| Mgi Id | MGI:3807415 | Doi | 10.1016/j.bbrc.2008.06.065 |
| Citation | Bourdi M, et al. (2008) Protective role of c-Jun N-terminal kinase 2 in acetaminophen-induced liver injury. Biochem Biophys Res Commun 374(1):6-10 |
| abstractText | Recent studies in mice suggest that stress-activated c-Jun N-terminal protein kinase 2 (JNK2) plays a pathologic role in acetaminophen (APAP)-induced liver injury (AILI), a major cause of acute liver failure (ALF). In contrast, we present evidence that JNK2 can have a protective role against AILI. When male C57BL/6J wild type (WT) and JNK2(-/-) mice were treated with 300mg APAP/kg, 90% of JNK2(-/-) mice died of ALF compared to 20% of WT mice within 48h. The high susceptibility of JNK2(-/-) mice to AILI appears to be due in part to deficiencies in hepatocyte proliferation and repair. Therefore, our findings are consistent with JNK2 signaling playing a protective role in AILI and further suggest that the use of JNK inhibitors as a potential treatment for AILI, as has been recommended by other investigators, should be reconsidered. |
