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Article: Attenuation of small-for-size liver graft injury by FTY720: Significance of cell survival Akt signaling pathway

TitleAttenuation of small-for-size liver graft injury by FTY720: Significance of cell survival Akt signaling pathway
Authors
KeywordsAkt survival pathway
FTY720
Liver transplantation
Small-for-size graft
Issue Date2004
PublisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/AJT
Citation
American Journal Of Transplantation, 2004, v. 4 n. 9, p. 1399-1407 How to Cite?
AbstractTo investigate the protective mechanism of FTY720 in small-for-size liver grafts, we applied a rat orthotopic liver transplantation model using 40% of liver grafts. FTY720 was administered (1 mg/kg, i.v.) at 20 min before graft harvesting in the donor, immediately before total hepatectomy and immediately after graft reperfusion in the recipient. The 7-day graft survival rates in the FTY720 group were significantly improved compared with the control group [100% (6/6) vs. 40% (4/10), p = 0.034]. FTY720 significantly reduced serum ALT and AST levels at 24 h after liver transplantation. The cell-survival Akt signaling pathway was activated in FTY720 groups by phosphorylation of Glycogen Synthase Kinase-3β, Bad and Forkhead Transcription Factor at 6 and 24 h after liver transplantation. The cleaved-caspases 3, 7 and 9 were down-regulated, accompanied with less apoptotic nuclei after FTY720 treatment. Acute-phase inflammatory MAPK pathway was down-regulated by dephosphorylation of c-Raf, Mek and Erk in the treatment groups. A20 and endothelial nitric oxide synthase were up-regulated together with down-regulation of iNOS. Hepatic sinusoids were well preserved in the FTY720 group but disrupted in the control group. In conclusion, FTY720 attenuates small-for-size liver graft injury by activation of cell-survival Akt signaling and down-regulation of the MAPK pathway.
Persistent Identifierhttp://hdl.handle.net/10722/148560
ISSN
2015 Impact Factor: 5.669
2015 SCImago Journal Rankings: 2.792
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhao, Yen_HK
dc.contributor.authorMan, Ken_HK
dc.contributor.authorLo, CMen_HK
dc.contributor.authorNg, KTen_HK
dc.contributor.authorLi, XLen_HK
dc.contributor.authorSun, CKen_HK
dc.contributor.authorLee, TKen_HK
dc.contributor.authorDai, XWen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2012-05-29T06:13:43Z-
dc.date.available2012-05-29T06:13:43Z-
dc.date.issued2004en_HK
dc.identifier.citationAmerican Journal Of Transplantation, 2004, v. 4 n. 9, p. 1399-1407en_HK
dc.identifier.issn1600-6135en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148560-
dc.description.abstractTo investigate the protective mechanism of FTY720 in small-for-size liver grafts, we applied a rat orthotopic liver transplantation model using 40% of liver grafts. FTY720 was administered (1 mg/kg, i.v.) at 20 min before graft harvesting in the donor, immediately before total hepatectomy and immediately after graft reperfusion in the recipient. The 7-day graft survival rates in the FTY720 group were significantly improved compared with the control group [100% (6/6) vs. 40% (4/10), p = 0.034]. FTY720 significantly reduced serum ALT and AST levels at 24 h after liver transplantation. The cell-survival Akt signaling pathway was activated in FTY720 groups by phosphorylation of Glycogen Synthase Kinase-3β, Bad and Forkhead Transcription Factor at 6 and 24 h after liver transplantation. The cleaved-caspases 3, 7 and 9 were down-regulated, accompanied with less apoptotic nuclei after FTY720 treatment. Acute-phase inflammatory MAPK pathway was down-regulated by dephosphorylation of c-Raf, Mek and Erk in the treatment groups. A20 and endothelial nitric oxide synthase were up-regulated together with down-regulation of iNOS. Hepatic sinusoids were well preserved in the FTY720 group but disrupted in the control group. In conclusion, FTY720 attenuates small-for-size liver graft injury by activation of cell-survival Akt signaling and down-regulation of the MAPK pathway.en_HK
dc.languageengen_US
dc.publisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/AJTen_HK
dc.relation.ispartofAmerican Journal of Transplantationen_HK
dc.subjectAkt survival pathwayen_HK
dc.subjectFTY720en_HK
dc.subjectLiver transplantationen_HK
dc.subjectSmall-for-size graften_HK
dc.subject.meshAlanine Transaminase - Blooden_US
dc.subject.meshAnimalsen_US
dc.subject.meshAspartate Aminotransferases - Blooden_US
dc.subject.meshGraft Survival - Drug Effects - Immunology - Physiologyen_US
dc.subject.meshImmunosuppressive Agents - Therapeutic Useen_US
dc.subject.meshLiver - Anatomy & Histologyen_US
dc.subject.meshLiver Transplantation - Immunologyen_US
dc.subject.meshMap Kinase Signaling System - Drug Effects - Physiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshPropylene Glycols - Therapeutic Useen_US
dc.subject.meshProtein-Serine-Threonine Kinases - Physiologyen_US
dc.subject.meshProtein-Tyrosine Kinases - Physiologyen_US
dc.subject.meshProto-Oncogene Proteins - Physiologyen_US
dc.subject.meshProto-Oncogene Proteins C-Akten_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Lewen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshSphingosine - Analogs & Derivativesen_US
dc.subject.meshTranscription Factors - Metabolismen_US
dc.subject.meshTransplantation, Homologousen_US
dc.titleAttenuation of small-for-size liver graft injury by FTY720: Significance of cell survival Akt signaling pathwayen_HK
dc.typeArticleen_HK
dc.identifier.emailMan, K: kwanman@hku.hken_HK
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hken_HK
dc.identifier.emailNg, KT: ledodes@hku.hken_HK
dc.identifier.emailLee, TK: tkwlee@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityMan, K=rp00417en_HK
dc.identifier.authorityLo, CM=rp00412en_HK
dc.identifier.authorityNg, KT=rp01720en_HK
dc.identifier.authorityLee, TK=rp00447en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1111/j.1600-6143.2004.00527.xen_HK
dc.identifier.pmid15307827-
dc.identifier.scopuseid_2-s2.0-4344581956en_HK
dc.identifier.hkuros90333-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-4344581956&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume4en_HK
dc.identifier.issue9en_HK
dc.identifier.spage1399en_HK
dc.identifier.epage1407en_HK
dc.identifier.isiWOS:000223283900003-
dc.publisher.placeDenmarken_HK
dc.identifier.scopusauthoridZhao, Y=7407402718en_HK
dc.identifier.scopusauthoridMan, K=7101754072en_HK
dc.identifier.scopusauthoridLo, CM=7401771672en_HK
dc.identifier.scopusauthoridNg, KT=7403178513en_HK
dc.identifier.scopusauthoridLi, XL=13008588500en_HK
dc.identifier.scopusauthoridSun, CK=7404248685en_HK
dc.identifier.scopusauthoridLee, TK=7501439435en_HK
dc.identifier.scopusauthoridDai, XW=8088837400en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK

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