Regulation of ghrelin receptor by microbial and inflammatory signals in human osteoblasts
Autor(a) principal: | |
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Data de Publicação: | 2019 |
Outros Autores: | , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Brazilian Oral Research |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1806-83242019000100221 |
Resumo: | Abstract: Recently, 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. |
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Regulation of ghrelin receptor by microbial and inflammatory signals in human osteoblastsReceptors, GhrelinGhrelinOsteoblastsPeriodontitisFusobacterium nucleatumAbstract: Recently, 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.Sociedade Brasileira de Pesquisa Odontológica - SBPqO2019-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S1806-83242019000100221Brazilian Oral Research v.33 2019reponame:Brazilian Oral Researchinstname:Sociedade Brasileira de Pesquisa Odontológica (SBPqO)instacron:SBPQO10.1590/1807-3107bor-2019.vol33.0025info:eu-repo/semantics/openAccessNokhbehsaim,MarjanNogueira,Andressa Vilas BoasMemmert,SvenjaDamanaki,AnnaEick,SigrunCirelli,Joni AugustoDeschner,Jameseng2019-07-01T00:00:00Zoai:scielo:S1806-83242019000100221Revistahttps://www.scielo.br/j/bor/https://old.scielo.br/oai/scielo-oai.phppob@edu.usp.br||bor@sbpqo.org.br1807-31071806-8324opendoar:2019-07-01T00:00Brazilian Oral Research - Sociedade Brasileira de Pesquisa Odontológica (SBPqO)false |
dc.title.none.fl_str_mv |
Regulation of ghrelin receptor by microbial and inflammatory signals in human osteoblasts |
title |
Regulation of ghrelin receptor by microbial and inflammatory signals in human osteoblasts |
spellingShingle |
Regulation of ghrelin receptor by microbial and inflammatory signals in human osteoblasts Nokhbehsaim,Marjan Receptors, Ghrelin Ghrelin Osteoblasts Periodontitis Fusobacterium nucleatum |
title_short |
Regulation of ghrelin receptor by microbial and inflammatory signals in human osteoblasts |
title_full |
Regulation of ghrelin receptor by microbial and inflammatory signals in human osteoblasts |
title_fullStr |
Regulation of ghrelin receptor by microbial and inflammatory signals in human osteoblasts |
title_full_unstemmed |
Regulation of ghrelin receptor by microbial and inflammatory signals in human osteoblasts |
title_sort |
Regulation of ghrelin receptor by microbial and inflammatory signals in human osteoblasts |
author |
Nokhbehsaim,Marjan |
author_facet |
Nokhbehsaim,Marjan Nogueira,Andressa Vilas Boas Memmert,Svenja Damanaki,Anna Eick,Sigrun Cirelli,Joni Augusto Deschner,James |
author_role |
author |
author2 |
Nogueira,Andressa Vilas Boas Memmert,Svenja Damanaki,Anna Eick,Sigrun Cirelli,Joni Augusto Deschner,James |
author2_role |
author author author author author author |
dc.contributor.author.fl_str_mv |
Nokhbehsaim,Marjan Nogueira,Andressa Vilas Boas Memmert,Svenja Damanaki,Anna Eick,Sigrun Cirelli,Joni Augusto Deschner,James |
dc.subject.por.fl_str_mv |
Receptors, Ghrelin Ghrelin Osteoblasts Periodontitis Fusobacterium nucleatum |
topic |
Receptors, Ghrelin Ghrelin Osteoblasts Periodontitis Fusobacterium nucleatum |
description |
Abstract: Recently, 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. |
publishDate |
2019 |
dc.date.none.fl_str_mv |
2019-01-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1806-83242019000100221 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1806-83242019000100221 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/1807-3107bor-2019.vol33.0025 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Sociedade Brasileira de Pesquisa Odontológica - SBPqO |
publisher.none.fl_str_mv |
Sociedade Brasileira de Pesquisa Odontológica - SBPqO |
dc.source.none.fl_str_mv |
Brazilian Oral Research v.33 2019 reponame:Brazilian Oral Research instname:Sociedade Brasileira de Pesquisa Odontológica (SBPqO) instacron:SBPQO |
instname_str |
Sociedade Brasileira de Pesquisa Odontológica (SBPqO) |
instacron_str |
SBPQO |
institution |
SBPQO |
reponame_str |
Brazilian Oral Research |
collection |
Brazilian Oral Research |
repository.name.fl_str_mv |
Brazilian Oral Research - Sociedade Brasileira de Pesquisa Odontológica (SBPqO) |
repository.mail.fl_str_mv |
pob@edu.usp.br||bor@sbpqo.org.br |
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1750318326246014976 |