Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10766554 | Biochemical and Biophysical Research Communications | 2008 | 5 Pages |
Abstract
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 JNK2â/â mice were treated with 300Â mg APAP/kg, 90% of JNK2â/â mice died of ALF compared to 20% of WT mice within 48Â h. The high susceptibility of JNK2â/â 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.
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Authors
Mohammed Bourdi, Midhun C. Korrapati, Mala Chakraborty, Steven B. Yee, Lance R. Pohl,