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dc.contributor.authorBartaula-Brevik, Sushmaen_US
dc.contributor.authorPedersen, Torbjorn Østviken_US
dc.contributor.authorBlois, Anna Len_US
dc.contributor.authorPapadakou, Panagiotaen_US
dc.contributor.authorFinne-Wistrand, Annaen_US
dc.contributor.authorXue, Yingen_US
dc.contributor.authorBolstad, Anne Isineen_US
dc.contributor.authorMustafa, Kamal Babikeir Elnen_US
dc.date.accessioned2015-02-19T08:49:12Z
dc.date.available2015-02-19T08:49:12Z
dc.date.issued2014-12-20eng
dc.identifier.issn1757-6512
dc.identifier.urihttp://hdl.handle.net/1956/9407
dc.description.abstractIntroduction Inflammation plays a crucial role in tissue regeneration, wound healing, and the success of tissue-engineered constructs. The aim of this study was to investigate the influence of human umbilical vein endothelial cells (ECs) on leukocyte transmigration when co-cultured with primary human bone marrow-derived multipotent stromal cells (MSCs). Methods MSCs with and without ECs were cultured in poly (L-lactide-co-1, 5-dioxepan-2-one) (poly (LLA-co-DXO)) scaffolds for 1 week in vitro in a bioreactor system, after which they were implanted subcutaneously in non-obese diabetic/severe combined immunodeficient mice. After 1 and 3 weeks, scaffolds were retrieved, and the mRNA expression of interleukin 1-beta (IL-1β), IL-6, IL-10, hypoxia-inducible factor 1-alpha (HIF-1α), HIF-1β, and mammalian target of rapamycin was examined by real-time reverse transcription-polymerase chain reaction. Furthermore, immunofluorescent staining was performed for IL-1β, IL-6, neutrophils, and CD11b. In addition, Western blotting was done for IL-1β and IL-6. Leukocyte transmigration genes and genes in Toll-like receptor pathways, expressed by MSCs cultured in vitro with or without ECs, were further investigated with a microarray dataset. Results In vitro, genes involved in leukocyte transmigration and Toll-like receptor pathways were clearly influenced by the addition of ECs. Platelet/endothelial cell adhesion molecule-1 (PECAM-1) and cadherin-5 (CDH5), both genes involved in leukocyte transmigration, were expressed significantly higher in the MSC/EC group. In vivo, the MSC/EC group showed higher mRNA expression of hypoxia-inducible factors HIF-1α and HIF-1β. The mRNA expression of anti-inflammatory cytokine IL-10 showed no significant difference, whereas the mRNA and protein expression of pro-inflammatory cytokines IL-1β and IL-6 were lower in the MSC/EC group. The quantitative analysis of immunofluorescent staining revealed a significant difference in the number of neutrophils migrating into constructs, with the highest density found in the MSC/EC group. The number of macrophages positive for IL-6 and CD11b was significantly reduced in the MSC/EC group. Conclusions The recruitment of leukocytes into tissue-engineered constructs with MSCs is strongly influenced by the addition of ECs via activation of leukocyte transmigration and Toll-like receptor pathways.en_US
dc.language.isoengeng
dc.publisherBioMed Centraleng
dc.relation.ispartof<a href="http://hdl.handle.net/1956/15230" target="blank">Vascularization and Host Response in Bone Tissue Engineering</a>
dc.rightsAttribution CC BYeng
dc.rights.urihttp://creativecommons.org/licenses/by/4.0eng
dc.titleLeukocyte transmigration into tissue-engineered constructs is influenced by endothelial cells through Toll-like receptor signalingen_US
dc.typePeer reviewed
dc.typeJournal article
dc.date.updated2015-02-03T12:24:27Z
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2014 Bartaula-Brevik et al.; licensee BioMed Central. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
dc.rights.holderSushma Bartaula-Brevik et al.; licensee BioMed Central Ltd.
dc.source.articlenumber143
dc.identifier.doihttps://doi.org/10.1186/scrt533
dc.identifier.cristin1188785
dc.source.journalStem Cell Research & Therapy
dc.source.405
dc.source.146


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