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Article: Allograft inflammatory factor-1 (AIF-1) is crucial for the survival and pro-inflammatory activity of macrophages

TitleAllograft inflammatory factor-1 (AIF-1) is crucial for the survival and pro-inflammatory activity of macrophages
Authors
KeywordsAllograft inflammatory factor-1
Macrophages
Issue Date2005
PublisherOxford University Press. The Journal's web site is located at http://intimm.oxfordjournals.org/
Citation
International Immunology, 2005, v. 17 n. 11, p. 1391-1397 How to Cite?
AbstractOur previous studies revealed that macrophages played an important role in linking injury, inflammatory and immune response in small-for-size liver transplantation. However, the molecular basis that promoted macrophage activation was not clear. In the present study, we explored the potential role of allograft inflammatory factor-1 (AIF-1) in mediating the survival and pro-inflammatory activity of macrophages in a macrophage cell line. First, the expression of AIF-1 was investigated with the stimulation of pro-inflammatory cytokines and anti-inflammatory treatment. Second, the level of inducible nitric oxide synthase (iNOS) and the survival and migration activity of macrophages were determined with the alterations of AIF-1 expression. Finally, a potential molecule that regulated AIF-1 expression was identified by the proteomic approach. The macrophage cell line expressed a certain level of endogenous AIF-1, which could be enhanced by pro-inflammatory cytokines IL-1β or tumor necrosis factor-α and suppressed by anti-inflammatory drug sodium salicylate. AIF-1 augmentation induced by AIF-1/PCDNA3.1(+) transfection enhanced the levels of iNOS and monocyte chemoattractant protein-1, and promoted the cell migration. On the other hand, suppression of AIF-1 expression by AIF-1/short interference RNA (siRNA) inhibited iNOS production, induced macrophage cell apoptosis and blocked the cell migration. Using two-dimensional electrophoresis, a disintegrin and metalloproteinase domain 3 (ADAM3) was identified after AIF-1/siRNA transfection. Transfection of ADAM3/ PCDNA3.1(+) up-regulated the expression of AIF-1 and iNOS, whereas suppression of ADAM3 expression down-regulated AIF-1 and iNOS expression. In conclusion, AIF-1 played an important role in the survival and pro-inflammatory activity of macrophages, and ADAM3 might be an upstream molecule that regulated AIF-1 expression. © The Japanese Society for Immunology 2005. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/84391
ISSN
2015 Impact Factor: 3.031
2015 SCImago Journal Rankings: 1.613
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYang, ZFen_HK
dc.contributor.authorHo, DWen_HK
dc.contributor.authorLau, CKen_HK
dc.contributor.authorLam, CTen_HK
dc.contributor.authorLum, CTen_HK
dc.contributor.authorPoon, RTPen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-06T08:52:23Z-
dc.date.available2010-09-06T08:52:23Z-
dc.date.issued2005en_HK
dc.identifier.citationInternational Immunology, 2005, v. 17 n. 11, p. 1391-1397en_HK
dc.identifier.issn0953-8178en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84391-
dc.description.abstractOur previous studies revealed that macrophages played an important role in linking injury, inflammatory and immune response in small-for-size liver transplantation. However, the molecular basis that promoted macrophage activation was not clear. In the present study, we explored the potential role of allograft inflammatory factor-1 (AIF-1) in mediating the survival and pro-inflammatory activity of macrophages in a macrophage cell line. First, the expression of AIF-1 was investigated with the stimulation of pro-inflammatory cytokines and anti-inflammatory treatment. Second, the level of inducible nitric oxide synthase (iNOS) and the survival and migration activity of macrophages were determined with the alterations of AIF-1 expression. Finally, a potential molecule that regulated AIF-1 expression was identified by the proteomic approach. The macrophage cell line expressed a certain level of endogenous AIF-1, which could be enhanced by pro-inflammatory cytokines IL-1β or tumor necrosis factor-α and suppressed by anti-inflammatory drug sodium salicylate. AIF-1 augmentation induced by AIF-1/PCDNA3.1(+) transfection enhanced the levels of iNOS and monocyte chemoattractant protein-1, and promoted the cell migration. On the other hand, suppression of AIF-1 expression by AIF-1/short interference RNA (siRNA) inhibited iNOS production, induced macrophage cell apoptosis and blocked the cell migration. Using two-dimensional electrophoresis, a disintegrin and metalloproteinase domain 3 (ADAM3) was identified after AIF-1/siRNA transfection. Transfection of ADAM3/ PCDNA3.1(+) up-regulated the expression of AIF-1 and iNOS, whereas suppression of ADAM3 expression down-regulated AIF-1 and iNOS expression. In conclusion, AIF-1 played an important role in the survival and pro-inflammatory activity of macrophages, and ADAM3 might be an upstream molecule that regulated AIF-1 expression. © The Japanese Society for Immunology 2005. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://intimm.oxfordjournals.org/en_HK
dc.relation.ispartofInternational Immunologyen_HK
dc.rightsInternational Immunology. Copyright © Oxford University Press.en_HK
dc.subjectAllograft inflammatory factor-1en_HK
dc.subjectMacrophagesen_HK
dc.titleAllograft inflammatory factor-1 (AIF-1) is crucial for the survival and pro-inflammatory activity of macrophagesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0953-8178&volume=17&issue=11&spage=1391&epage=1397&date=2005&atitle=Allograft+inflammatory+factor-1+(AIF-1)+is+crucial+for+the+survival+and+pro-inflammatory+activity+of+macrophagesen_HK
dc.identifier.emailLum, CT: ctlum@graduate.hku.hken_HK
dc.identifier.emailPoon, RTP: poontp@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityLum, CT=rp00757en_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1093/intimm/dxh316en_HK
dc.identifier.pmid16157606-
dc.identifier.scopuseid_2-s2.0-27744490848en_HK
dc.identifier.hkuros116940en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-27744490848&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume17en_HK
dc.identifier.issue11en_HK
dc.identifier.spage1391en_HK
dc.identifier.epage1397en_HK
dc.identifier.isiWOS:000232749600003-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridYang, ZF=14018809600en_HK
dc.identifier.scopusauthoridHo, DW=7402971906en_HK
dc.identifier.scopusauthoridLau, CK=7401968442en_HK
dc.identifier.scopusauthoridLam, CT=7402989860en_HK
dc.identifier.scopusauthoridLum, CT=7006889374en_HK
dc.identifier.scopusauthoridPoon, RTP=7103097223en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.citeulike355998-

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