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Article: Biliverdin, a natural product of heme catabolism, induces tolerance to cardiac allografts

TitleBiliverdin, a natural product of heme catabolism, induces tolerance to cardiac allografts
Authors
Issue Date2004
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
The FASEB Journal, 2004, v. 18 n. 6, p. 765-767 How to Cite?
AbstractBiliverdin, a product of heme oxygenase-1 (HO-1) enzymatic action, is converted into bilirubin, which has been considered a waste product in the past. We now show that administration of biliverdin has a salutary effect in organ transplantation. A brief course of treatment with biliverdin leads to long-term survival of H-2 incompatible heart allografts. Furthermore, those recipients harboring long-surviving (>100 days) allografts were tolerant to donor antigens indicated by the acceptance of second donor strain hearts but not third-party grafts. Treatment with biliverdin decreased intragraft leukocyte infiltration and inhibited T cell proliferation. Likely related to tolerance induction, biliverdin interferes with T cell signaling by inhibiting activation of nuclear factor of activated T cells (NFAT) and nuclear factor kappaB (NF-kappaB), two transcription factors involved in interleukin-2 (IL-2) transcription and T cell proliferation, as well as suppressing Th1 interferon-gamma (IFN-gamma) production in vitro. These findings support the potential use of biliverdin, a natural product, in transplantation and other T cell mediated immune disorders.
Persistent Identifierhttp://hdl.handle.net/10722/224586
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorYamashita, K-
dc.contributor.authorMcDaid, J-
dc.contributor.authorOllinger, RO-
dc.contributor.authorTsui, TY-
dc.contributor.authorBerberat, PO-
dc.contributor.authorUsheva, A-
dc.contributor.authorCsizmadia, E-
dc.contributor.authorSmith, RN-
dc.contributor.authorSoares, MP-
dc.contributor.authorBach, FH-
dc.date.accessioned2016-04-08T03:46:35Z-
dc.date.available2016-04-08T03:46:35Z-
dc.date.issued2004-
dc.identifier.citationThe FASEB Journal, 2004, v. 18 n. 6, p. 765-767-
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/224586-
dc.description.abstractBiliverdin, a product of heme oxygenase-1 (HO-1) enzymatic action, is converted into bilirubin, which has been considered a waste product in the past. We now show that administration of biliverdin has a salutary effect in organ transplantation. A brief course of treatment with biliverdin leads to long-term survival of H-2 incompatible heart allografts. Furthermore, those recipients harboring long-surviving (>100 days) allografts were tolerant to donor antigens indicated by the acceptance of second donor strain hearts but not third-party grafts. Treatment with biliverdin decreased intragraft leukocyte infiltration and inhibited T cell proliferation. Likely related to tolerance induction, biliverdin interferes with T cell signaling by inhibiting activation of nuclear factor of activated T cells (NFAT) and nuclear factor kappaB (NF-kappaB), two transcription factors involved in interleukin-2 (IL-2) transcription and T cell proliferation, as well as suppressing Th1 interferon-gamma (IFN-gamma) production in vitro. These findings support the potential use of biliverdin, a natural product, in transplantation and other T cell mediated immune disorders.-
dc.languageeng-
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/-
dc.relation.ispartofThe FASEB Journal-
dc.subject.meshBiliverdine - metabolism - pharmacology - therapeutic use-
dc.subject.meshHeart Transplantation - immunology - pathology-
dc.subject.meshNuclear Proteins-
dc.subject.meshT-Lymphocytes - drug effects - immunology-
dc.subject.meshTransplantation Toleranc-
dc.titleBiliverdin, a natural product of heme catabolism, induces tolerance to cardiac allografts-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1096/fj.03-0839fje-
dc.identifier.pmid14977878-
dc.identifier.hkuros89297-
dc.identifier.volume18-
dc.identifier.issue6-
dc.identifier.spage765-
dc.identifier.epage767-
dc.publisher.placeUnited States-

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