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Article: The influence of phosphatidylinositol 3-kinase/Akt pathway on the ischemic injury during rat liver graft preservation

TitleThe influence of phosphatidylinositol 3-kinase/Akt pathway on the ischemic injury during rat liver graft preservation
Authors
KeywordsCaspase
Ischemic injury
Organ preservation
PI3-kinase/Akt
Issue Date2005
PublisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/AJT
Citation
American Journal Of Transplantation, 2005, v. 5 n. 6, p. 1264-1275 How to Cite?
AbstractWe aimed to investigate the role of phosphatidylinositol 3 (PI3)-kinase/Akt pathway on ischemic injury. Rat liver grafts were preserved in UW solution with different treatments and were compared by 1-week survival rates and morphological changes with those of the control group. PI3-kinase/Akt was significantly activated at the sites of Thr 308 and Ser 473 in the preserved grafts. Downstream target proteins, glycogen synthase kinase-3β (GSK-3β) and caspase-9, were inactivated. However, survival signal transduction from Akt to Bad was blocked by calcium release after activation of PI3-kinase/Akt. Significant activation of caspase-12, -3 and -7 contributed to cell apoptosis and severe ischemic injury was shown after 7 h of preservation by UW solution with insulin. Downregulation of phospho-Akt at Thr 308 and Ser 473 was due to partial inhibition of PI3-kinase/Akt pathway by LY294002. Activation of GSK-3β and inactivation of caspase-12 and Bad could be found in the LY294002 groups in which the liver grafts showed less ischemic injury. Higher 1-week survival rates in the heparin, LY294002, and glucagon groups confirmed the dysregulation of the pathway. In conclusion, PI3-kinase/Akt pathway was dysregulated and contributed to ischemic injury during preservation. Heparin and LY294002 could improve graft viability by maintaining calcium homeostasis during preservation. Copyright © Blackwell Munksgaard 2005.
Persistent Identifierhttp://hdl.handle.net/10722/83841
ISSN
2015 Impact Factor: 5.669
2015 SCImago Journal Rankings: 2.792
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, XLen_HK
dc.contributor.authorMan, Ken_HK
dc.contributor.authorNg, KTen_HK
dc.contributor.authorSun, CKen_HK
dc.contributor.authorLo, CMen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-06T08:45:52Z-
dc.date.available2010-09-06T08:45:52Z-
dc.date.issued2005en_HK
dc.identifier.citationAmerican Journal Of Transplantation, 2005, v. 5 n. 6, p. 1264-1275en_HK
dc.identifier.issn1600-6135en_HK
dc.identifier.urihttp://hdl.handle.net/10722/83841-
dc.description.abstractWe aimed to investigate the role of phosphatidylinositol 3 (PI3)-kinase/Akt pathway on ischemic injury. Rat liver grafts were preserved in UW solution with different treatments and were compared by 1-week survival rates and morphological changes with those of the control group. PI3-kinase/Akt was significantly activated at the sites of Thr 308 and Ser 473 in the preserved grafts. Downstream target proteins, glycogen synthase kinase-3β (GSK-3β) and caspase-9, were inactivated. However, survival signal transduction from Akt to Bad was blocked by calcium release after activation of PI3-kinase/Akt. Significant activation of caspase-12, -3 and -7 contributed to cell apoptosis and severe ischemic injury was shown after 7 h of preservation by UW solution with insulin. Downregulation of phospho-Akt at Thr 308 and Ser 473 was due to partial inhibition of PI3-kinase/Akt pathway by LY294002. Activation of GSK-3β and inactivation of caspase-12 and Bad could be found in the LY294002 groups in which the liver grafts showed less ischemic injury. Higher 1-week survival rates in the heparin, LY294002, and glucagon groups confirmed the dysregulation of the pathway. In conclusion, PI3-kinase/Akt pathway was dysregulated and contributed to ischemic injury during preservation. Heparin and LY294002 could improve graft viability by maintaining calcium homeostasis during preservation. Copyright © Blackwell Munksgaard 2005.en_HK
dc.languageengen_HK
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.subjectCaspaseen_HK
dc.subjectIschemic injuryen_HK
dc.subjectOrgan preservationen_HK
dc.subjectPI3-kinase/Akten_HK
dc.titleThe influence of phosphatidylinositol 3-kinase/Akt pathway on the ischemic injury during rat liver graft preservationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1600-6135&volume=5&issue=6&spage=1264&epage=1275&date=2005&atitle=The+influence+of+phosphatidylinositol+3-kinase/Akt+pathway+on+the+ischemic+injury+during+rat+liver+graft+preservationen_HK
dc.identifier.emailMan, K: kwanman@hku.hken_HK
dc.identifier.emailNg, KT: ledodes@hku.hken_HK
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityMan, K=rp00417en_HK
dc.identifier.authorityNg, KT=rp01720en_HK
dc.identifier.authorityLo, CM=rp00412en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1600-6143.2005.00877.xen_HK
dc.identifier.pmid15888030-
dc.identifier.scopuseid_2-s2.0-20544447208en_HK
dc.identifier.hkuros97956en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-20544447208&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume5en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1264en_HK
dc.identifier.epage1275en_HK
dc.identifier.isiWOS:000229031400012-
dc.publisher.placeDenmarken_HK
dc.identifier.scopusauthoridLi, XL=13008588500en_HK
dc.identifier.scopusauthoridMan, K=7101754072en_HK
dc.identifier.scopusauthoridNg, KT=7403178513en_HK
dc.identifier.scopusauthoridSun, CK=7404248685en_HK
dc.identifier.scopusauthoridLo, CM=7401771672en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.citeulike199161-

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