File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Rosiglitazone suppresses cyclosporin-induced chronic transplant dysfunction and prolongs survival of rat cardiac allografts

TitleRosiglitazone suppresses cyclosporin-induced chronic transplant dysfunction and prolongs survival of rat cardiac allografts
Authors
KeywordsAtherosclerosis
Cardiac allografts
Chronic transplant dysfunction
PPAR agonists
Issue Date2007
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.transplantjournal.com
Citation
Transplantation, 2007, v. 83 n. 12, p. 1602-1610 How to Cite?
AbstractBACKGROUND. The lack of effective treatment for chronic transplant dysfunction restricts the long-term survival of solid organ allografts. Peroxisome proliferator-activated receptor ligands can suppress vascular inflammation. The aim of this study was to analyze the effects of rosiglitazone on chronic transplant dysfunction in a rat cardiac transplant model. METHODS. Inbred male Fisher 344 (F344, RT1) and Lewis (LEW, RT1) rats were subjected to heterotopic abdominal heart transplantation according to standard procedures. Cyclosporine A was administered intraperitoneally to cover acute rejection, and rosiglitazone was administered orally by gavage daily from 3 days before the operation to the end of experiments. RESULTS. Rosiglitazone significantly prolonged the survival of cardiac allografts in rats (F344 to LEW) that had received a 10-day course of cyclosporin A compared to treatment with immunosuppressant alone. Analysis of allografts at 120 days posttransplantation showed that rosiglitazone reduced the inflammatory cell infiltrate in both the vessels and graft parenchyma as were neointimal formation, vascular occlusion, and fibrosis. Expression of transforming growth factor-β and related proteins was less abundant after cyclosporin A/rosiglitazone treatment. CONCLUSIONS. The findings reported here demonstrate that rosiglitazone given under the cover of short-term treatment with cyclosporin A prolongs cardiac allograft survival and reduces the severity of chronic transplant dysfunction. This may be mediated in part through the downregulation of transforming growth factor-β and related proteins. The combined effects of rosiglitazone and immunosuppressive drugs are potentially beneficial to patients receiving organ transplants. © 2007 Lippincott Williams & Wilkins, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/83741
ISSN
2015 Impact Factor: 3.69
2015 SCImago Journal Rankings: 1.699
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, Yen_HK
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorYuan, Zen_HK
dc.contributor.authorTian, Len_HK
dc.contributor.authorDallman, MJen_HK
dc.contributor.authorThompson, PWen_HK
dc.contributor.authorTam, PKHen_HK
dc.contributor.authorLamb, JRen_HK
dc.date.accessioned2010-09-06T08:44:39Z-
dc.date.available2010-09-06T08:44:39Z-
dc.date.issued2007en_HK
dc.identifier.citationTransplantation, 2007, v. 83 n. 12, p. 1602-1610en_HK
dc.identifier.issn0041-1337en_HK
dc.identifier.urihttp://hdl.handle.net/10722/83741-
dc.description.abstractBACKGROUND. The lack of effective treatment for chronic transplant dysfunction restricts the long-term survival of solid organ allografts. Peroxisome proliferator-activated receptor ligands can suppress vascular inflammation. The aim of this study was to analyze the effects of rosiglitazone on chronic transplant dysfunction in a rat cardiac transplant model. METHODS. Inbred male Fisher 344 (F344, RT1) and Lewis (LEW, RT1) rats were subjected to heterotopic abdominal heart transplantation according to standard procedures. Cyclosporine A was administered intraperitoneally to cover acute rejection, and rosiglitazone was administered orally by gavage daily from 3 days before the operation to the end of experiments. RESULTS. Rosiglitazone significantly prolonged the survival of cardiac allografts in rats (F344 to LEW) that had received a 10-day course of cyclosporin A compared to treatment with immunosuppressant alone. Analysis of allografts at 120 days posttransplantation showed that rosiglitazone reduced the inflammatory cell infiltrate in both the vessels and graft parenchyma as were neointimal formation, vascular occlusion, and fibrosis. Expression of transforming growth factor-β and related proteins was less abundant after cyclosporin A/rosiglitazone treatment. CONCLUSIONS. The findings reported here demonstrate that rosiglitazone given under the cover of short-term treatment with cyclosporin A prolongs cardiac allograft survival and reduces the severity of chronic transplant dysfunction. This may be mediated in part through the downregulation of transforming growth factor-β and related proteins. The combined effects of rosiglitazone and immunosuppressive drugs are potentially beneficial to patients receiving organ transplants. © 2007 Lippincott Williams & Wilkins, Inc.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.transplantjournal.comen_HK
dc.relation.ispartofTransplantationen_HK
dc.subjectAtherosclerosisen_HK
dc.subjectCardiac allograftsen_HK
dc.subjectChronic transplant dysfunctionen_HK
dc.subjectPPAR agonistsen_HK
dc.subject.meshCyclosporine - adverse effects-
dc.subject.meshGraft Survival - drug effects-
dc.subject.meshHeart Transplantation - immunology - pathology-
dc.subject.meshThiazolidinediones - therapeutic use-
dc.subject.meshVasodilator Agents - therapeutic use-
dc.titleRosiglitazone suppresses cyclosporin-induced chronic transplant dysfunction and prolongs survival of rat cardiac allograftsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0041-1337&volume=83&issue=12&spage=1602&epage=1610&date=2007&atitle=Rosiglitazone+suppresses+cyclosporin-induced+chronic+transplant+dysfunction+and+prolongs+survival+of+rat+cardiac+allograftsen_HK
dc.identifier.emailChen, Y:ychenc@hkucc.hku.hken_HK
dc.identifier.emailTam, PKH:paultam@hkucc.hku.hken_HK
dc.identifier.authorityChen, Y=rp01318en_HK
dc.identifier.authorityTam, PKH=rp00060en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/01.tp.0000266994.39480.42en_HK
dc.identifier.pmid17589344-
dc.identifier.scopuseid_2-s2.0-34250839390en_HK
dc.identifier.hkuros135744en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34250839390&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume83en_HK
dc.identifier.issue12en_HK
dc.identifier.spage1602en_HK
dc.identifier.epage1610en_HK
dc.identifier.isiWOS:000247578200014-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChen, Y=36463185300en_HK
dc.identifier.scopusauthoridLiu, Y=25928027200en_HK
dc.identifier.scopusauthoridYuan, Z=10641253300en_HK
dc.identifier.scopusauthoridTian, L=7202296389en_HK
dc.identifier.scopusauthoridDallman, MJ=35473592200en_HK
dc.identifier.scopusauthoridThompson, PW=7403220269en_HK
dc.identifier.scopusauthoridTam, PKH=7202539421en_HK
dc.identifier.scopusauthoridLamb, JR=7201524642en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats