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Regular Article |
-Mediated Hepatocyte Apoptosis and Liver Injury
From the Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, Minnesota
Tumor necrosis factor-
(TNF-) contributes to liver injury by
inducing hepatocyte apoptosis. Recent evidence suggests that cathepsin
B (cat B) contributes to TNF--induced apoptosis in
vitro. The aim of the present study was to determine whether
cat B contributes to TNF--induced hepatocyte apoptosis and liver
injury in vivo. Cat B knockout
(catB-/-) and wild-type
(catB+/+) mice were first infected with the
adenovirus Ad5I
B expressing the IB superrepressor to
inhibit nuclear factor-B-induced survival signals and then treated
with murine recombinant TNF-. Massive hepatocyte apoptosis with
mitochondrial release of cytochrome c and activation of
caspases 9 and 3 was detected in catB+/+
mice 2 hours after the injection of TNF-. In
contrast, significantly less hepatocyte apoptosis and no
detectable release of cytochrome c or caspase activation
occurred in the livers of catB-/- mice. By
4 hours after TNF- injection, only 20% of the
catB+/+ mice were alive as compared to
85% of catB-/- mice.
Pharmacological inhibition of cat B in
catB+/+ mice with
L-3-trans-(propylcarbamoyl)oxirane-2-carbonyl-L-isoleucyl-L-proline
(CA-074 Me) also reduced TNF--induced liver damage. The present data
demonstrate that a cat B-mitochondrial apoptotic pathway plays a
pivotal role in TNF--induced hepatocyte apoptosis and liver
injury.
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