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World J Gastroenterol. Dec 28, 2014; 20(48): 18189-18198
Published online Dec 28, 2014. doi: 10.3748/wjg.v20.i48.18189
Published online Dec 28, 2014. doi: 10.3748/wjg.v20.i48.18189
Caspase-12 mediates carbon tetrachloride-induced hepatocyte apoptosis in mice
Hua Liu, Michael J Nowicki, Division of Pediatric Gastroenterology, University of Mississippi Medical Center, Jackson, MS 39216, United States
Zhe Wang, Cancer Institute, University of Mississippi Medical Center, Jackson, MS 39216, United States
Author contributions: Liu H and Wang Z performed the research, analyzed the data, and drafted the article; Liu H and Nowicki MJ designed the study, and edited, revised, and gave final approval to the article.
Supported by Institutional research grant by the University of Mississippi Medical Center (to Dr. Hua Liu), No. 68512250711
Correspondence to: Hua Liu, MD, Division of Gastroenterology, Department of Pediatrics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216, United States. hliu@umc.edu
Telephone: +1-601-9845978 Fax: +1-601-9845981
Received: May 6, 2014
Revised: July 3, 2014
Accepted: September 5, 2014
Published online: December 28, 2014
Revised: July 3, 2014
Accepted: September 5, 2014
Published online: December 28, 2014
Core Tip
Core tip: Sublethal doses of carbon tetrachloride (CCl4) induced significant hepatocyte apoptosis and acute liver injury in the wild-type mice. CCl4 also induced the generation of reactive oxygen species in the liver followed by activation of caspase-12, -9 and -3. Loss of caspase-12 in knock-out mice attenuated CCl4-induced activation of caspase-9 and -3, significantly reduced apoptosis, and preserved liver function. Caspase-8 was not detected, indicating that it does not play a significant role in this model of hepatocyte apoptosis. The data indicate that caspase-12 plays a pivotal role in CCl4-induced hepatocyte apoptosis through the downstream activation of the effector caspase-3 directly and/or indirectly via caspase-9 activation.