Hypoxia?İnduced Endothelial Cell Responses – Possible Roles During Periodontal Disease

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dc.authorid10721en_US
dc.contributor.authorPamuk, Ferda
dc.contributor.authorHasturk, Hatice
dc.contributor.authorKantarci, Alpdogan
dc.contributor.authorMendes, Reila T.
dc.contributor.authorNguyen, Daniel
dc.contributor.authorFernandes, Daniel
dc.contributor.authorVan Dyke, Thomas E.
dc.contributor.authorStephens, Danielle
dc.date.accessioned2019-03-28T06:46:26Z
dc.date.available2019-03-28T06:46:26Z
dc.date.issued2018
dc.departmentİstanbul Beykent Üniversitesien_US
dc.description.abstractBackground and objective Inflammatory periodontal pockets are known to be hypoxic. Hypoxia influences vascular response to periodontal inflammation, including angiogenesis, which is critical for oxygen and nutrient delivery to periodontal tissues and granulation tissue formation. Our previous work suggests that periodontal bacteria may actively contribute to pocket hypoxia. Herein, we test the hypothesis that Fusobacterium nucleatum actively induces low oxygen tension, which modulates angiogenesis and endothelial cell activity. HUVEC cells were incubated in 1.5% oxygen for (Folkman & Shing, 1992)48 hours. Cell proliferation was measured by MTT; surface expression of CD31, CD34 and VEGF receptors (VEGFR1, VEGFR2) were analyzed by FACS. mRNA expression of HIF isoforms, iNOS, eNOS, COX?2, and VEGF was measured by quantitative PCR. Supernatants were analyzed for the release of IL?1?, TNF??, and VEGF by ELISA or multiplex immunoassays and nitric oxide was measured by colorimetric assay. F. nucleatum actively depleted oxygen. Hypoxia resulted in a significant increase of HIF isoforms. iNOS was increased while nitric oxide was unchanged. VEGF release was increased at 4 hours followed by an increase in VEGFR1 at 12 hours, but not VEGFR2. CD31 expression was reduced and CD34 was increased after 48 hours (p < 0.05). IL?1? and TNF?? release were decreased at 4 hours (p < 0.05), but both increased by 24 hours; TNF?? increased at 24 h. The data highlight the role of hypoxia in endothelial cell inflammatory changes. F. nucleatum, considered a bridging species in the development of periodontopathic biofilms induces hypoxia in the periodontium leading to angiogenic changes in periodontal disease pathogenesisen_US
dc.identifier.doi10.1002/cre2.135
dc.identifier.issn2057-4347
dc.identifier.pmid30603105en_US
dc.identifier.scopus2-s2.0-85058452247en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1002/cre2.135
dc.identifier.wosWOS:000454298500003en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileytr_TR
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.subjectendothelial cells,tr_TR
dc.subjectFusobacterium nucleatumtr_TR
dc.subjectinflammationtr_TR
dc.subjectoxygentr_TR
dc.subjectperiodontitistr_TR
dc.titleHypoxia?İnduced Endothelial Cell Responses – Possible Roles During Periodontal Diseaseen_US
dc.typeArticleen_US

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