Heme oxygenase-1 induction in hepatocytes and non-parenchymal cells protects against liver injury during endotoxemia

Persistent Link:
http://hdl.handle.net/10150/610124
Title:
Heme oxygenase-1 induction in hepatocytes and non-parenchymal cells protects against liver injury during endotoxemia
Author:
Dorman, Robert; Bajt, Mary; Farhood, Anwar; Mayes, January; Jaeschke, Hartmut
Affiliation:
Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA; Liver Research Institute, University of Arizona, 1501 N. Campbell Avenue, Tucson, Arizona 85724, USA; Department of Pathology, University of Texas Health Science Center, Houston, Texas 77030, USA
Issue Date:
2004
Publisher:
BioMed Central
Citation:
Comparative Hepatology 2004, 3(Suppl 1):S42 http://www.comparative-hepatology.com/content/3/S1/S42
Journal:
Comparative Hepatology
Rights:
©  Dorman et al; licensee BioMed Central Ltd 2004
Collection Information:
This item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.
Abstract:
INTRODUCTION:Heme oxygenase-1 (HO-1) is a stress response enzyme, which catalyses the breakdown of heme into biliverdin-IX alpha, carbon monoxide and ferrous iron. Under situations of oxidative stress, heat stress, ischemia/reperfusion injury or endotoxemia, HO-1 has been shown to be induced and to elicit a protective effect. The mechanism of how this protective effect is executed is unknown.RESULTS:HO-1 induction with cobalt protoporphorin (Co-PP) dose-dependently protected against apoptotic cell death as well as neutrophil-mediated oncosis in the galactosamine/endotoxin (Gal/ET) shock model. Induction of HO-1 with Co-PP dose-dependently protected against neutrophil-mediated oncosis as indicated by attenuated ALT release and TNF-mediated apoptotic cell death as indicated by reduced caspase-3 activation. HO-1 induction did not attenuate Gal/ET-induced TNF-alpha formation. Furthermore, a similar protective effect with the high dose of Co-PP was observed when animals were treated with Gal/TNF-alpha.CONCLUSIONS:HO-1 induction attenuates apoptosis and neutrophil-mediated oncosis in the Gal/ET shock model. However, the protective effect is not due to the reduction of TNF-alpha release or the attenuation of neutrophil accumulation in the liver sinusoids.
EISSN:
1476-5926
DOI:
10.1186/1476-5926-2-S1-S42
Version:
Final published version
Additional Links:
http://www.comparative-hepatology.com/content/3/S1/S42

Full metadata record

DC FieldValue Language
dc.contributor.authorDorman, Roberten
dc.contributor.authorBajt, Maryen
dc.contributor.authorFarhood, Anwaren
dc.contributor.authorMayes, Januaryen
dc.contributor.authorJaeschke, Hartmuten
dc.date.accessioned2016-05-20T08:59:07Z-
dc.date.available2016-05-20T08:59:07Z-
dc.date.issued2004en
dc.identifier.citationComparative Hepatology 2004, 3(Suppl 1):S42 http://www.comparative-hepatology.com/content/3/S1/S42en
dc.identifier.doi10.1186/1476-5926-2-S1-S42en
dc.identifier.urihttp://hdl.handle.net/10150/610124-
dc.description.abstractINTRODUCTION:Heme oxygenase-1 (HO-1) is a stress response enzyme, which catalyses the breakdown of heme into biliverdin-IX alpha, carbon monoxide and ferrous iron. Under situations of oxidative stress, heat stress, ischemia/reperfusion injury or endotoxemia, HO-1 has been shown to be induced and to elicit a protective effect. The mechanism of how this protective effect is executed is unknown.RESULTS:HO-1 induction with cobalt protoporphorin (Co-PP) dose-dependently protected against apoptotic cell death as well as neutrophil-mediated oncosis in the galactosamine/endotoxin (Gal/ET) shock model. Induction of HO-1 with Co-PP dose-dependently protected against neutrophil-mediated oncosis as indicated by attenuated ALT release and TNF-mediated apoptotic cell death as indicated by reduced caspase-3 activation. HO-1 induction did not attenuate Gal/ET-induced TNF-alpha formation. Furthermore, a similar protective effect with the high dose of Co-PP was observed when animals were treated with Gal/TNF-alpha.CONCLUSIONS:HO-1 induction attenuates apoptosis and neutrophil-mediated oncosis in the Gal/ET shock model. However, the protective effect is not due to the reduction of TNF-alpha release or the attenuation of neutrophil accumulation in the liver sinusoids.en
dc.language.isoenen
dc.publisherBioMed Centralen
dc.relation.urlhttp://www.comparative-hepatology.com/content/3/S1/S42en
dc.rights©  Dorman et al; licensee BioMed Central Ltd 2004en
dc.titleHeme oxygenase-1 induction in hepatocytes and non-parenchymal cells protects against liver injury during endotoxemiaen
dc.typeArticleen
dc.identifier.eissn1476-5926en
dc.contributor.departmentDepartment of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USAen
dc.contributor.departmentLiver Research Institute, University of Arizona, 1501 N. Campbell Avenue, Tucson, Arizona 85724, USAen
dc.contributor.departmentDepartment of Pathology, University of Texas Health Science Center, Houston, Texas 77030, USAen
dc.identifier.journalComparative Hepatologyen
dc.description.collectioninformationThis item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.en
dc.eprint.versionFinal published versionen
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