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Conference Paper: Modulation of heme oxygenase in tissue injury and its implication in protection against gastrointestinal diseases

TitleModulation of heme oxygenase in tissue injury and its implication in protection against gastrointestinal diseases
Authors
KeywordsHeme oxygenase
Tissue injury
Inflammation
Gastrointestinal diseases
Issue Date2001
Citation
The 3rd International Symposium on Cell/Tissue Injury and Cytoprotection/Organoprotection, Long Beach, CA., 24-27 February 2000. In Life Sciences, 2001, v. 69, n. 25-26, p. 3113-3119 How to Cite?
AbstractHeme oxygenase (HO) is the rate-limiting enzyme in the catabolism of heme, followed by production of biliverdin, free iron and carbon monoxide (CO). There are three isoforms of HO: HO-1 is highly inducible, whereas HO-2 and HO-3 are constitutively expressed. In addition to heme, a variety of nonheme compounds, including heavy metals, cytokines, endotoxins and heat shock stress are strong inducers of HO-1 expression. Many studies indicated that induction of HO-1 is associated with a protective response due to the removal of free heme, which is shown to be toxic. However, recent studies demonstrated that the expression of HO-1 in response to different inflammatory mediators could contribute in part to the resolution of inflammation and have protective effects on brain, liver, kidney and lung against injuries. These beneficial effects seem to be due to the production of bile pigment biliverdin and bilirubin that is a potent antioxidant, as well as the release of iron and CO. However, there are few studies concerning the relationship between HO-1 and inflammation as well as injury in the gut. Interestingly, a preliminary study implicated that induction of HO-1 expression in a colonic damage model induced by trinitrobenzene sulfonic acid played a critical protective role, indicating that activation of HO-1 could act as a natural defensive mechanism to alleviate inflammation and tissue injury in the gastrointestinal tract. © Elsevier Science Inc. All rights reserved.
DescriptionThese journal issues contain invited, peer-reviewed papers written by participants of the 3rd International Symposium on Cell/Tissue Injury and Cytoprotection/Organoprotection (Long Beach, CA, February 24–27, 2000).
Persistent Identifierhttp://hdl.handle.net/10722/207484
ISSN
2015 Impact Factor: 2.685
2015 SCImago Journal Rankings: 1.056

 

DC FieldValueLanguage
dc.contributor.authorGuo, Xin-
dc.contributor.authorShin, Vivianyvonne-
dc.contributor.authorCho, Chihin-
dc.date.accessioned2014-12-31T01:01:46Z-
dc.date.available2014-12-31T01:01:46Z-
dc.date.issued2001-
dc.identifier.citationThe 3rd International Symposium on Cell/Tissue Injury and Cytoprotection/Organoprotection, Long Beach, CA., 24-27 February 2000. In Life Sciences, 2001, v. 69, n. 25-26, p. 3113-3119-
dc.identifier.issn0024-3205-
dc.identifier.urihttp://hdl.handle.net/10722/207484-
dc.descriptionThese journal issues contain invited, peer-reviewed papers written by participants of the 3rd International Symposium on Cell/Tissue Injury and Cytoprotection/Organoprotection (Long Beach, CA, February 24–27, 2000).-
dc.description.abstractHeme oxygenase (HO) is the rate-limiting enzyme in the catabolism of heme, followed by production of biliverdin, free iron and carbon monoxide (CO). There are three isoforms of HO: HO-1 is highly inducible, whereas HO-2 and HO-3 are constitutively expressed. In addition to heme, a variety of nonheme compounds, including heavy metals, cytokines, endotoxins and heat shock stress are strong inducers of HO-1 expression. Many studies indicated that induction of HO-1 is associated with a protective response due to the removal of free heme, which is shown to be toxic. However, recent studies demonstrated that the expression of HO-1 in response to different inflammatory mediators could contribute in part to the resolution of inflammation and have protective effects on brain, liver, kidney and lung against injuries. These beneficial effects seem to be due to the production of bile pigment biliverdin and bilirubin that is a potent antioxidant, as well as the release of iron and CO. However, there are few studies concerning the relationship between HO-1 and inflammation as well as injury in the gut. Interestingly, a preliminary study implicated that induction of HO-1 expression in a colonic damage model induced by trinitrobenzene sulfonic acid played a critical protective role, indicating that activation of HO-1 could act as a natural defensive mechanism to alleviate inflammation and tissue injury in the gastrointestinal tract. © Elsevier Science Inc. All rights reserved.-
dc.languageeng-
dc.relation.ispartofLife Sciences-
dc.subjectHeme oxygenase-
dc.subjectTissue injury-
dc.subjectInflammation-
dc.subjectGastrointestinal diseases-
dc.titleModulation of heme oxygenase in tissue injury and its implication in protection against gastrointestinal diseases-
dc.typeConference_Paper-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0024-3205(01)01417-5-
dc.identifier.pmid11758836-
dc.identifier.scopuseid_2-s2.0-0035834304-
dc.identifier.hkuros73400-
dc.identifier.volume69-
dc.identifier.issue25-26-
dc.identifier.spage3113-
dc.identifier.epage3119-
dc.customcontrol.immutablesml 160617 amended-

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