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Regulation of ghrelin receptor by microbial and inflammatory signals in human osteoblasts

dc.contributor.authorNokhbehsaim, Marjan
dc.contributor.authorNogueira, Andressa Vilas Boas
dc.contributor.authorMemmert, Svenja
dc.contributor.authorDamanaki, Anna
dc.contributor.authorEick, Sigrun
dc.contributor.authorCirelli, Joni Augusto [UNESP]
dc.contributor.authorDeschner, James
dc.contributor.institutionSection of Experimental Dento-Maxillo-Facial Medicine
dc.contributor.institutionJohannes Gutenberg University
dc.contributor.institutionCenter of Dento-Maxillo-Facial Medicine
dc.contributor.institutionLaboratory of Oral Microbiology
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2019-10-06T16:29:44Z
dc.date.available2019-10-06T16:29:44Z
dc.date.issued2019-04-25
dc.description.abstractRecently, it has been suggested that the anti-inflammatory hormone ghrelin (GHRL) and its receptor GHS-R may play a pivotal role in periodontal health and diseases. However, their exact regulation and effects in periodontitis are not known. The aim of this in-vitro study was to investigate the effect of microbial and inflammatory insults on the GHS-R1a expression in human osteoblast-like cells. MG-63 cells were exposed to interleukin (IL)-1β and Fusobacterium nucleatum in the presence and absence of GHRL for up to 2 d. Subsequently, gene expressions of GHS-R1a, inflammatory mediators and matrix metalloproteinase were analyzed by real-time PCR. GHS-R protein synthesis and NF-κB p65 nuclear translocation were assessed by immunocytochemistry and immunofluorescence microscopy, respectively. IL-1β and F. nucleatum caused a significant upregulation of GHS-R1a expression and an increase in GHS-R1a protein. Pre-incubation with a MEK1/2 inhibitor diminished the IL-1β-induced GHS-R1a upregulation. IL-1β and F. nucleatum also enhanced the expressions of cyclooxygenase 2, CC-chemokine ligand 2, IL-6, IL-8, and matrix metalloproteinase 1, but these stimulatory effects were counteracted by GHRL. By contrast, the stimulatory actions of IL-1β and F. nucleatum on the GHS-R1a expression were further enhanced by GHRL. Our study provides original evidence that IL-1β and F. nucleatum regulate the GHS-R/GHRL system in osteoblast-like cells. Furthermore, we demonstrate for the first time that the proinflammatory and proteolytic actions of IL-1β and F. nucleatum on osteoblast-like cells are inhibited by GHRL. Our study suggests that microbial and inflammatory insults upregulate GHS-R1a, which may represent a protective negative feedback mechanism in human bone.en
dc.description.affiliationUniversity of Bonn Center of Dento-Maxillo-Facial Medicine Section of Experimental Dento-Maxillo-Facial Medicine
dc.description.affiliationUniversity Medical Center Johannes Gutenberg University Department of Periodontology and Operative Dentistry
dc.description.affiliationUniversity of Bonn Center of Dento-Maxillo-Facial Medicine Department of Orthodontics
dc.description.affiliationUniversity of Bern Department of Periodontology Laboratory of Oral Microbiology
dc.description.affiliationUniversidade Estadual Paulista - UNESP School of Dentistry of Araraquara Department of Diagnosis and Surgery
dc.description.affiliationUnespUniversidade Estadual Paulista - UNESP School of Dentistry of Araraquara Department of Diagnosis and Surgery
dc.format.extente025
dc.identifierhttp://dx.doi.org/10.1590/1807-3107bor-2019.vol33.0025
dc.identifier.citationBrazilian oral research, v. 33, p. e025-.
dc.identifier.doi10.1590/1807-3107bor-2019.vol33.0025
dc.identifier.fileS1806-83242019000100221.pdf
dc.identifier.issn1807-3107
dc.identifier.scieloS1806-83242019000100221
dc.identifier.scopus2-s2.0-85065481659
dc.identifier.urihttp://hdl.handle.net/11449/189100
dc.language.isoeng
dc.relation.ispartofBrazilian oral research
dc.rights.accessRightsAcesso abertopt
dc.sourceScopus
dc.titleRegulation of ghrelin receptor by microbial and inflammatory signals in human osteoblastsen
dc.typeArtigopt
dspace.entity.typePublication
relation.isOrgUnitOfPublicationca4c0298-cd82-48ee-a9c8-c97704bac2b0
relation.isOrgUnitOfPublication.latestForDiscoveryca4c0298-cd82-48ee-a9c8-c97704bac2b0
unesp.author.orcid0000-0003-0998-1717[1]
unesp.author.orcid0000-0002-2756-5947[2]
unesp.author.orcid0000-0002-8153-6610[3]
unesp.author.orcid0000-0002-2706-398X[4]
unesp.author.orcid0000-0002-4619-2461[5]
unesp.author.orcid0000-0002-7082-9290[6]
unesp.author.orcid0000-0002-8808-8769[7]
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Odontologia, Araraquarapt
unesp.departmentDiagnóstico e Cirurgia - FOARpt

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