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Conference Paper: Monocytic U937 adhesion, tumor necrosis factor-alpha and interleukin-1 beta expression in response to gelatin-based networks grafted with arginine-glycine-aspartic acid and proline-histidine-serine-arginine-asparagine oligopeptides

TitleMonocytic U937 adhesion, tumor necrosis factor-alpha and interleukin-1 beta expression in response to gelatin-based networks grafted with arginine-glycine-aspartic acid and proline-histidine-serine-arginine-asparagine oligopeptides
Authors
Issue Date2007
Citation
Tissue Engineering, 2007, v. 13, n. 1, p. 179-185 How to Cite?
AbstractIn this study we synthesized gelatin-based, tissue-engineering, interpenetrating network (IPN) scaffolds immobilized with fibronectin (FN)-derived peptides to assess monocyte-biomaterial interaction. Human promonocytic U937 cells were seeded onto peptide-grafted IPN or tissue-culture polystyrene plate (TCPS) pre-adsorbed with FN or FN-derived peptides. The presence of RGD influenced U937 density on IPN. Interleuldn-1 beta (IL-1β) messenger ribonucleic acid (mRNA) expression in adherent U937 on treated TCPS was slightly upregulated at 4h. Tumor necrosis factor alpha (TNF-α) and IL-1β mRNA expression in adherent U937 on all IPNs was generally downregulated at 4 h. This downregulation of IL-1β mRNA apparently varied in IPNs grafted with different ligand and was still present at 24 h. TNF-α and IL-1β proteins released from U937 on treated TCPS were comparable with the control at 24 h, but TNF-α and IL-1β protein expression in U937 on IPNs was lower at 24 h than on the TCPS control. The results indicate that the tissue-engineering substrate and the bioactive peptides modulate the initial U937 adhesion and the subsequent inflammatory cytokine gene and protein expression. © Mary Ann Liebert, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/216187
ISSN
2013 Impact Factor: 4.254
2010 SCImago Journal Rankings: 1.962

 

DC FieldValueLanguage
dc.contributor.authorGao, Qiang-
dc.contributor.authorChung, Amy S.-
dc.contributor.authorKao, Weiyuan John-
dc.date.accessioned2015-08-25T10:22:17Z-
dc.date.available2015-08-25T10:22:17Z-
dc.date.issued2007-
dc.identifier.citationTissue Engineering, 2007, v. 13, n. 1, p. 179-185-
dc.identifier.issn1076-3279-
dc.identifier.urihttp://hdl.handle.net/10722/216187-
dc.description.abstractIn this study we synthesized gelatin-based, tissue-engineering, interpenetrating network (IPN) scaffolds immobilized with fibronectin (FN)-derived peptides to assess monocyte-biomaterial interaction. Human promonocytic U937 cells were seeded onto peptide-grafted IPN or tissue-culture polystyrene plate (TCPS) pre-adsorbed with FN or FN-derived peptides. The presence of RGD influenced U937 density on IPN. Interleuldn-1 beta (IL-1β) messenger ribonucleic acid (mRNA) expression in adherent U937 on treated TCPS was slightly upregulated at 4h. Tumor necrosis factor alpha (TNF-α) and IL-1β mRNA expression in adherent U937 on all IPNs was generally downregulated at 4 h. This downregulation of IL-1β mRNA apparently varied in IPNs grafted with different ligand and was still present at 24 h. TNF-α and IL-1β proteins released from U937 on treated TCPS were comparable with the control at 24 h, but TNF-α and IL-1β protein expression in U937 on IPNs was lower at 24 h than on the TCPS control. The results indicate that the tissue-engineering substrate and the bioactive peptides modulate the initial U937 adhesion and the subsequent inflammatory cytokine gene and protein expression. © Mary Ann Liebert, Inc.-
dc.languageeng-
dc.relation.ispartofTissue Engineering-
dc.titleMonocytic U937 adhesion, tumor necrosis factor-alpha and interleukin-1 beta expression in response to gelatin-based networks grafted with arginine-glycine-aspartic acid and proline-histidine-serine-arginine-asparagine oligopeptides-
dc.typeConference_Paper-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1089/ten.2006.0007-
dc.identifier.pmid17518591-
dc.identifier.scopuseid_2-s2.0-33846580014-
dc.identifier.volume13-
dc.identifier.issue1-
dc.identifier.spage179-
dc.identifier.epage185-

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