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Article: Insulin-like growth factor-1 treatment prevents anti-fas antibody-induced apoptosis in endplate chondrocytes

TitleInsulin-like growth factor-1 treatment prevents anti-fas antibody-induced apoptosis in endplate chondrocytes
Authors
Issue Date2006
PublisherLippincott, Williams & Wilkins. The Journal's web site is located at http://www.spinejournal.com
Citation
Spine, 2006, v. 31 n. 7, p. 736-741 How to Cite?
AbstractStudy Design. In vitro investigation of vertebral endplate chondrocyte apoptosis. Objectives. To determine whether Fas antibody caused apoptosis in endplate chondrocytes, and whether insulin-like growth factor-1 (IGF-1) inhibited this effect. Integrin-ā1 and focal adhesion kinase (FAK) expression in conjunction with apoptosis was also investigated. Summary of Background Data. Binding of Fas antibody to Fas mimics Fas-FasL ligation, which causes apoptosis. IGF-1 has been shown to have anti-apoptotic effects. Materials and Methods. Rat cervical endplate chondrocytes were cultured and treated with Fas antibody, with or without IGF-1. Cellular morphology was examined by microscopy. Apoptotic changes were evaluated by transmission electron microscopy, TUNEL staining, and immunostaining. Apoptosis-induced changes in the expression of integrin-ā1 chain and FAK were also investigated. Results. Endplate chondrocytes were able to be cultured; a chondrocytic phenotype was maintained. Fas antibody induced apoptosis in endplate chondrocytes; this was confirmed by TUNEL staining. Bcl-2 expression was decreased by Fas antibody, while Bax expression increased. Integrin-ā1 and FAK expression was decreased by Fas antibody. IGF-1 treatment inhibited these Fas antibody-induced changes. Conclusions. Fas antibody induces apoptosis and decreases Integrin-ā1 and FAK expression in cultured endplate chondrocytes; IGF-1 is protective against these changes. ©2006, Lippincott Williams & Wilkins, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/170082
ISSN
2015 Impact Factor: 2.439
2015 SCImago Journal Rankings: 1.459
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, YJen_US
dc.contributor.authorShi, Qen_US
dc.contributor.authorSun, Pen_US
dc.contributor.authorZhou, Qen_US
dc.contributor.authorDarowish, Men_US
dc.contributor.authorLi, TFen_US
dc.contributor.authorDong, YFen_US
dc.contributor.authorLu, WWen_US
dc.contributor.authorLeong, JCYen_US
dc.date.accessioned2012-10-30T06:05:13Z-
dc.date.available2012-10-30T06:05:13Z-
dc.date.issued2006en_US
dc.identifier.citationSpine, 2006, v. 31 n. 7, p. 736-741en_US
dc.identifier.issn0362-2436en_US
dc.identifier.urihttp://hdl.handle.net/10722/170082-
dc.description.abstractStudy Design. In vitro investigation of vertebral endplate chondrocyte apoptosis. Objectives. To determine whether Fas antibody caused apoptosis in endplate chondrocytes, and whether insulin-like growth factor-1 (IGF-1) inhibited this effect. Integrin-ā1 and focal adhesion kinase (FAK) expression in conjunction with apoptosis was also investigated. Summary of Background Data. Binding of Fas antibody to Fas mimics Fas-FasL ligation, which causes apoptosis. IGF-1 has been shown to have anti-apoptotic effects. Materials and Methods. Rat cervical endplate chondrocytes were cultured and treated with Fas antibody, with or without IGF-1. Cellular morphology was examined by microscopy. Apoptotic changes were evaluated by transmission electron microscopy, TUNEL staining, and immunostaining. Apoptosis-induced changes in the expression of integrin-ā1 chain and FAK were also investigated. Results. Endplate chondrocytes were able to be cultured; a chondrocytic phenotype was maintained. Fas antibody induced apoptosis in endplate chondrocytes; this was confirmed by TUNEL staining. Bcl-2 expression was decreased by Fas antibody, while Bax expression increased. Integrin-ā1 and FAK expression was decreased by Fas antibody. IGF-1 treatment inhibited these Fas antibody-induced changes. Conclusions. Fas antibody induces apoptosis and decreases Integrin-ā1 and FAK expression in cultured endplate chondrocytes; IGF-1 is protective against these changes. ©2006, Lippincott Williams & Wilkins, Inc.en_US
dc.languageengen_US
dc.publisherLippincott, Williams & Wilkins. The Journal's web site is located at http://www.spinejournal.comen_US
dc.relation.ispartofSpineen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntibodies, Monoclonal - Metabolism - Physiologyen_US
dc.subject.meshAntibody Affinityen_US
dc.subject.meshAntigens, Cd95 - Immunology - Metabolismen_US
dc.subject.meshApoptosis - Drug Effects - Physiologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshChondrocytes - Cytology - Drug Effects - Metabolismen_US
dc.subject.meshFas Ligand Proteinen_US
dc.subject.meshInsulin-Like Growth Factor I - Pharmacologyen_US
dc.subject.meshIntegrin Alpha1 - Biosynthesisen_US
dc.subject.meshMembrane Glycoproteins - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshTumor Necrosis Factors - Metabolismen_US
dc.titleInsulin-like growth factor-1 treatment prevents anti-fas antibody-induced apoptosis in endplate chondrocytesen_US
dc.typeArticleen_US
dc.identifier.emailLu, WW:wwlu@hku.hken_US
dc.identifier.authorityLu, WW=rp00411en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/01.brs.0000208128.49912.64en_US
dc.identifier.pmid16582846-
dc.identifier.scopuseid_2-s2.0-33645797829en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33645797829&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume31en_US
dc.identifier.issue7en_US
dc.identifier.spage736en_US
dc.identifier.epage741en_US
dc.identifier.isiWOS:000236579800003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWang, YJ=8320879700en_US
dc.identifier.scopusauthoridShi, Q=7402698372en_US
dc.identifier.scopusauthoridSun, P=55126448500en_US
dc.identifier.scopusauthoridZhou, Q=52465006800en_US
dc.identifier.scopusauthoridDarowish, M=10540863300en_US
dc.identifier.scopusauthoridLi, TF=8360236800en_US
dc.identifier.scopusauthoridDong, YF=8853270700en_US
dc.identifier.scopusauthoridLu, WW=7404215221en_US
dc.identifier.scopusauthoridLeong, JCY=35560782200en_US

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