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Conference Paper: NLRP3 inflammasome regulated by telomere-independent Repressor Activator Protein1(RAP1) induced graft injury after LDLT

TitleNLRP3 inflammasome regulated by telomere-independent Repressor Activator Protein1(RAP1) induced graft injury after LDLT
Authors
KeywordsMedical sciences
Gastroenterology medical sciences
Surgery
Issue Date2014
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jtoc/106570021
Citation
The 2014 Joint International Congress of ILTS, ELITA and LICAGE, London, UK., 4-7 June 2014. In Liver Transplantation, 2014, v. 20 suppl. S1, p. S252, abstract P-326 How to Cite?
AbstractBACKGROUND AND OBJECTIVE: Inflammasomes, a multi-molecular complex in the cytoplasm, can activate caspase-1 which subsequently processes the secretion of interleukin-b (IL-1b) and IL-18. The role of inflammasomes and the regulation mechanism after liver transplantation remains unclear. Here, we aim to explore the role and mechanism of inflammasomes on liver graft injury after Living Donor Liver Transplantation (LDLT). MATERIALS AND METHODS: The expression pattern of inflammasomes and its association with RAP1, IL-1b was investigated in the patients after LDLT, rat orthotopic liver transplantation models and mouse hepatic ischemia/reperfusion model with major hepatectomy (50%). The regulating role of RAP1 on NLRP3 inflammasome was also validated in RAP1-/- mice. The underlying mechanism was further explored in the primary macrophages isolated from RAP1-/- mice. RESULTS: The intragraft expression of NLRP3 was significantly up-regulated at 2 hours after reperfusion accompanied by the increase of RAP1 and IL-1b (NLRP3: 5.96; RAP1:3.21; IL-1b:4.34 folds of normal liver) in human liver grafts. Consistently, the hepatic expression of NLRP3 was significantly higher at 2 hours after reperfusion in mice (3.66 folds of the normal liver), and correlated with macrophage infiltration, hepatic necrosis and increasing secretion of inflammatory chemokines and cytokines. In RAP1-/- mice, the expression of NLRP3 and IL-1b was significantly down-regulated compared to wild type controls(NLRP3: 3.66 vs 1.95, p=0.04; IL-1b: 5.71 vs 1.46 folds of the normal liver, p=0.01).
DescriptionPoster Session 2: P-326
This journal suppl. entitled: The ILTS 20th Annual International Congress
Persistent Identifierhttp://hdl.handle.net/10722/204490
ISSN
2015 Impact Factor: 3.951
2015 SCImago Journal Rankings: 1.763

 

DC FieldValueLanguage
dc.contributor.authorLiu, H-
dc.contributor.authorMan, K-
dc.contributor.authorLi, C-
dc.contributor.authorNg, KTP-
dc.contributor.authorLiu, X-
dc.contributor.authorGeng, W-
dc.contributor.authorQi, X-
dc.contributor.authorMA, YY-
dc.contributor.authorYeung, WH-
dc.contributor.authorLiu, J-
dc.contributor.authorLi, X-
dc.contributor.authorChan, SC-
dc.contributor.authorLo, CM-
dc.date.accessioned2014-09-19T23:57:03Z-
dc.date.available2014-09-19T23:57:03Z-
dc.date.issued2014-
dc.identifier.citationThe 2014 Joint International Congress of ILTS, ELITA and LICAGE, London, UK., 4-7 June 2014. In Liver Transplantation, 2014, v. 20 suppl. S1, p. S252, abstract P-326-
dc.identifier.issn1527-6465-
dc.identifier.urihttp://hdl.handle.net/10722/204490-
dc.descriptionPoster Session 2: P-326-
dc.descriptionThis journal suppl. entitled: The ILTS 20th Annual International Congress-
dc.description.abstractBACKGROUND AND OBJECTIVE: Inflammasomes, a multi-molecular complex in the cytoplasm, can activate caspase-1 which subsequently processes the secretion of interleukin-b (IL-1b) and IL-18. The role of inflammasomes and the regulation mechanism after liver transplantation remains unclear. Here, we aim to explore the role and mechanism of inflammasomes on liver graft injury after Living Donor Liver Transplantation (LDLT). MATERIALS AND METHODS: The expression pattern of inflammasomes and its association with RAP1, IL-1b was investigated in the patients after LDLT, rat orthotopic liver transplantation models and mouse hepatic ischemia/reperfusion model with major hepatectomy (50%). The regulating role of RAP1 on NLRP3 inflammasome was also validated in RAP1-/- mice. The underlying mechanism was further explored in the primary macrophages isolated from RAP1-/- mice. RESULTS: The intragraft expression of NLRP3 was significantly up-regulated at 2 hours after reperfusion accompanied by the increase of RAP1 and IL-1b (NLRP3: 5.96; RAP1:3.21; IL-1b:4.34 folds of normal liver) in human liver grafts. Consistently, the hepatic expression of NLRP3 was significantly higher at 2 hours after reperfusion in mice (3.66 folds of the normal liver), and correlated with macrophage infiltration, hepatic necrosis and increasing secretion of inflammatory chemokines and cytokines. In RAP1-/- mice, the expression of NLRP3 and IL-1b was significantly down-regulated compared to wild type controls(NLRP3: 3.66 vs 1.95, p=0.04; IL-1b: 5.71 vs 1.46 folds of the normal liver, p=0.01).-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jtoc/106570021-
dc.relation.ispartofLiver Transplantation-
dc.rightsLiver Transplantation. Copyright © John Wiley & Sons, Inc.-
dc.subjectMedical sciences-
dc.subjectGastroenterology medical sciences-
dc.subjectSurgery-
dc.titleNLRP3 inflammasome regulated by telomere-independent Repressor Activator Protein1(RAP1) induced graft injury after LDLT-
dc.typeConference_Paper-
dc.identifier.emailMan, K: kwanman@hku.hk-
dc.identifier.emailNg, KTP: ledodes@hku.hk-
dc.identifier.emailLiu, X: liuxb301@hku.hk-
dc.identifier.emailGeng, W: weigeng@hku.hk-
dc.identifier.emailQi, X: qixiang515@connect.hku.hk-
dc.identifier.emailYeung, WH: why21@hku.hk-
dc.identifier.emailChan, SC: chanlsc@hkucc.hku.hk-
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hk-
dc.identifier.authorityMan, K=rp00417-
dc.identifier.authorityNg, KTP=rp01720-
dc.identifier.authorityChan, SC=rp01568-
dc.identifier.authorityLo, CM=rp00412-
dc.identifier.doi10.1002/lt.23901-
dc.identifier.hkuros237557-
dc.identifier.volume20-
dc.identifier.issuesuppl. S1-
dc.identifier.spageS252, abstract P-326-
dc.identifier.epageS252, abstract P-326-
dc.publisher.placeUnited States-

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