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© Research
Publication : The Journal of biological chemistry

JunD protects the liver from ischemia/reperfusion injury by dampening AP-1 transcriptional activation

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in The Journal of biological chemistry - 08 Jan 2008

Marden JJ, Zhang Y, Oakley FD, Zhou W, Luo M, Jia HP, McCray PB, Yaniv M, Weitzman JB, Engelhardt JF

Link to Pubmed [PMID] – 18182393

J. Biol. Chem. 2008 Mar;283(11):6687-95

The AP-1 transcription factor modulates a wide range of cellular processes, including cellular proliferation, programmed cell death, and survival. JunD is a major component of the AP-1 complex following liver ischemia/reperfusion (I/R) injury; however, its precise function in this setting remains unclear. We investigated the functional significance of JunD in regulating AP-1 transcription following partial lobar I/R injury to the liver, as well as the downstream consequences for hepatocellular remodeling. Our findings demonstrate that JunD plays a protective role, reducing I/R injury to the liver by suppressing acute transcriptional activation of AP-1. In the absence of JunD, c-Jun phosphorylation and AP-1 activation in response to I/R injury were elevated, and this correlated with increased caspase activation, injury, and alterations in hepatocyte proliferation. The expression of dominant negative JNK1 inhibited c-Jun phosphorylation, AP-1 activation, and hepatic injury following I/R in JunD-/- mice but, paradoxically, led to an enhancement of AP-1 activation and liver injury in JunD+/- littermates. Enhanced JunD/JNK1-dependent liver injury correlated with the acute induction of diphenylene iodonium-sensitive NADPH-dependent superoxide production by the liver following I/R. In this context, dominant negative JNK1 expression elevated both Nox2 and Nox4 mRNA levels in the liver in a JunD-dependent manner. These findings suggest that JunD counterbalances JNK1 activation and the downstream redox-dependent hepatic injury that results from I/R, and may do so by regulating NADPH oxidases.

http://www.ncbi.nlm.nih.gov/pubmed/18182393