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Article: rAAV-mediated stable expression of heme oxygenase-1 in stellate cells: A new approach to attenuate liver fibrosis in rats

TitlerAAV-mediated stable expression of heme oxygenase-1 in stellate cells: A new approach to attenuate liver fibrosis in rats
Authors
Issue Date2005
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
Hepatology, 2005, v. 42 n. 2, p. 335-342 How to Cite?
AbstractLiver fibrosis is the consequence of activation of hepatic stellate cells mediated by persistent or recurrent liver injury, where oxidative stress or inflammatory response resulting from immune cells and cytokines are involved. Targeting of hepatic stellate cells could be an important strategy for the therapy of liver fibrosis. In this study, we showed a tropism of recombinant adeno-associated virus (rAAV, serotype 2) with high efficiency in transduction of a homeostatic gene, heme oxygenase-1 (HO-1), to activated stellate cells. The binding of rAAVs to stellate cells increased significantly after serum-stimulated activation compared with quiescent status. Portal injection of rAAVs to normal or carbon tetrachloride (CCl 4)-induced liver fibrosis showed a distinct distribution of rAAV binding. The majority of injected rAAVs bound to the cells in fibrotic areas that were associated with higher expression levels of fibroblast growth factor receptor-1α at 2 hours after administration. Isolation of different types of cells from CCl 4-induced fibrotic livers showed predominant expression of transgene in stellate cells after rAAV/HO-1 administration on day 3 and remained stable for 12 weeks. In addition, HO-1-transduced stellate cells showed reduced transcript levels of type 1 collagen and impaired proliferative ability compared with controls. With this approach, the severity of established micronodular cirrhosis was markedly reduced. In conclusion, these findings suggest a new approach for the treatment of liver fibrosis using adeno-associated virus-mediated gene transfer. Copyright © 2005 by the American Association for the Study of Liver Diseases.
Persistent Identifierhttp://hdl.handle.net/10722/83193
ISSN
2015 Impact Factor: 11.711
2015 SCImago Journal Rankings: 4.752
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTsui, TYen_HK
dc.contributor.authorLau, CKen_HK
dc.contributor.authorMa, Jen_HK
dc.contributor.authorWu, Xen_HK
dc.contributor.authorWang, YQen_HK
dc.contributor.authorFarkas, Sen_HK
dc.contributor.authorXu, Ren_HK
dc.contributor.authorSchlitt, HJen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-06T08:38:07Z-
dc.date.available2010-09-06T08:38:07Z-
dc.date.issued2005en_HK
dc.identifier.citationHepatology, 2005, v. 42 n. 2, p. 335-342en_HK
dc.identifier.issn0270-9139en_HK
dc.identifier.urihttp://hdl.handle.net/10722/83193-
dc.description.abstractLiver fibrosis is the consequence of activation of hepatic stellate cells mediated by persistent or recurrent liver injury, where oxidative stress or inflammatory response resulting from immune cells and cytokines are involved. Targeting of hepatic stellate cells could be an important strategy for the therapy of liver fibrosis. In this study, we showed a tropism of recombinant adeno-associated virus (rAAV, serotype 2) with high efficiency in transduction of a homeostatic gene, heme oxygenase-1 (HO-1), to activated stellate cells. The binding of rAAVs to stellate cells increased significantly after serum-stimulated activation compared with quiescent status. Portal injection of rAAVs to normal or carbon tetrachloride (CCl 4)-induced liver fibrosis showed a distinct distribution of rAAV binding. The majority of injected rAAVs bound to the cells in fibrotic areas that were associated with higher expression levels of fibroblast growth factor receptor-1α at 2 hours after administration. Isolation of different types of cells from CCl 4-induced fibrotic livers showed predominant expression of transgene in stellate cells after rAAV/HO-1 administration on day 3 and remained stable for 12 weeks. In addition, HO-1-transduced stellate cells showed reduced transcript levels of type 1 collagen and impaired proliferative ability compared with controls. With this approach, the severity of established micronodular cirrhosis was markedly reduced. In conclusion, these findings suggest a new approach for the treatment of liver fibrosis using adeno-associated virus-mediated gene transfer. Copyright © 2005 by the American Association for the Study of Liver Diseases.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/en_HK
dc.relation.ispartofHepatologyen_HK
dc.rightsHepatology. Copyright © John Wiley & Sons, Inc.en_HK
dc.titlerAAV-mediated stable expression of heme oxygenase-1 in stellate cells: A new approach to attenuate liver fibrosis in ratsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0270-9139&volume=42&issue=2&spage=335&epage=342&date=2005&atitle=rAAV-mediated+stable+expression+of+heme+oxygenase-1+in+stellate+cells:+a+new+approach+to+attenuate+liver+fibrosis+in+ratsen_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/hep.20803en_HK
dc.identifier.pmid16025519-
dc.identifier.scopuseid_2-s2.0-23044485967en_HK
dc.identifier.hkuros116932en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-23044485967&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume42en_HK
dc.identifier.issue2en_HK
dc.identifier.spage335en_HK
dc.identifier.epage342en_HK
dc.identifier.isiWOS:000230864900013-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTsui, TY=7006622455en_HK
dc.identifier.scopusauthoridLau, CK=7401968442en_HK
dc.identifier.scopusauthoridMa, J=7406201578en_HK
dc.identifier.scopusauthoridWu, X=7408231534en_HK
dc.identifier.scopusauthoridWang, YQ=23981317400en_HK
dc.identifier.scopusauthoridFarkas, S=7006093907en_HK
dc.identifier.scopusauthoridXu, R=7402813857en_HK
dc.identifier.scopusauthoridSchlitt, HJ=7005572464en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK

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