Protection of rat hepatocytes from apoptosis by inhibition of c-Jun N-terminal kinase.

Abstract:

BACKGROUND:Apoptotic cell death and c-Jun N-terminal kinase (JNK) activation occur after hepatic ischemia/reperfusion injury. In other cell types, JNK activation was shown to be required for apoptosis. This study tested the hypotheses that JNK contributes to hepatocellular apoptosis, and that inhibition of JNK activity improves cell viability. METHODS:Rat hepatocytes were harvested from Sprague-Dawley rats and pretreated with SP600125, a JNK inhibitor. Subsequently, they were exposed to apoptotic stimuli consisting of either the bile salt glycochenodeoxycholic acid (GCDC) or tumor necrosis factor (TNF)-alpha and actinomycin D. RESULTS:Western blotting demonstrated specific inhibition of JNK by SP600125. Inhibition of JNK resulted in improved viability measured with crystal violet, decreased in situ DNA nick end labeling positivity, and decreased cleavage of poly (ADP-ribose) polymerase and caspase-3. TNF-alpha and actinomycin D induced apoptosis, upregulated p53, and downregulated expression of the anti-apoptotic protein X-linked inhibitor of apoptosis protein. These effects were abrogated by JNK inhibition. CONCLUSIONS:These data show that pharmacologic inhibition of JNK activity reduces bile salt or TNF-alpha-induced apoptosis by maintaining expression of anti-apoptotic proteins. The results indicate that JNK is an important component of the apoptosis signaling cascade and suggest a possible therapeutic strategy in certain liver disorders.

journal_name

Surgery

journal_title

Surgery

authors

Marderstein EL,Bucher B,Guo Z,Feng X,Reid K,Geller DA

doi

10.1067/msy.2003.237

subject

Has Abstract

pub_date

2003-08-01 00:00:00

pages

280-4

issue

2

eissn

0039-6060

issn

1532-7361

pii

S0039606003002058

journal_volume

134

pub_type

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