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dc.contributor.authorIndrelid, Stine Hufthammer
dc.contributor.authorDongre, Harsh Nitin
dc.contributor.authorNunes, Ivana Pereira
dc.contributor.authorVirtej, Anca
dc.contributor.authorBletsa, Athanasia
dc.contributor.authorBerggreen, Ellen
dc.date.accessioned2023-12-28T10:34:29Z
dc.date.available2023-12-28T10:34:29Z
dc.date.created2023-03-21T15:12:46Z
dc.date.issued2023
dc.identifier.issn0022-3484
dc.identifier.urihttps://hdl.handle.net/11250/3108988
dc.description.abstractObjective The aim of this study was to investigate the response of gingival epithelial cells to microbial and inflammatory signals. Background The gingival epithelial barrier provides the first line of defense and supports tissue homeostasis by maintaining the cross-talk between gingival epithelium, oral microbiota, and immune cells. Lymphatic vessels are essential to sustaining this homeostasis. The gingival epithelial cells have been shown to produce prolymphangiogenic factors during physiologic conditions, but their role in response to microbial and inflammatory signals is unknown. Methods Immortalized human gingival epithelial cells (HGEC) and human dermal lymphatic microvascular endothelial cells (LEC) were cultured. HGEC were exposed to Porphyromonas gingivalis derived-LPS, human IL-1 beta/IL-1F2 protein, or recombinant human IL-6/IL-6R. Levels of vascular growth factors (VEGF-A, VEGF-C, and VEGF-D) in cell supernatants were determined by ELISA. LEC were grown to confluence, and a scratch was induced in the monolayer. Uncovered area was measured up to 48 h after exposure to conditioned medium (CM) from HGEC. Tube formation assays were performed with LEC cocultured with labelled HGEC or exposed to CM. Results VEGF-A, VEGF-C, and low levels of VEGF-D were constitutively expressed by HGEC. The expression of VEGF-C and VEGF-D, but not VEGF-A, was upregulated in response to proinflammatory mediators. VEGF-C was upregulated in response to P. gingivalis LPS, but not to Escherichia coli LPS. A scratch migration assay showed that LEC migration was significantly increased by CM from HGEC. Both the CM and coculture with HGEC induced significant tube formation of LEC. Conclusions HGEC can regulate production of lymphangiogenic/angiogenic factors during inflammatory insults and can stimulate proliferation, migration, and tube formation of LEC in vitro in a paracrine manner.en_US
dc.language.isoengen_US
dc.publisherWileyen_US
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/deed.no*
dc.titleHuman gingival epithelial cells stimulate proliferation, migration, and tube formation of lymphatic endothelial cells in vitroen_US
dc.typeJournal articleen_US
dc.typePeer revieweden_US
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2023 The Author(s)en_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.doi10.1111/jre.13110
dc.identifier.cristin2135871
dc.source.journalJournal of Periodontal Researchen_US
dc.source.pagenumber596-606en_US
dc.identifier.citationJournal of Periodontal Research. 2023, 58 (3), 596-606.en_US
dc.source.volume58en_US
dc.source.issue3en_US


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Attribution-NonCommercial-NoDerivatives 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivatives 4.0 Internasjonal