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

Nokhbehsaim, Marjan; Nogueira, Andressa Vilas Boas; Memmert, Svenja; Damanaki, Anna; Eick, Sigrun; Cirelli, Joni Augusto; Deschner, James (2019). Regulation of ghrelin receptor by microbial and inflammatory signals in human osteoblasts. Brazilian oral research, 33, e025. Sociedade Brasileira de Pesquisa Odontológica 10.1590/1807-3107bor-2019.vol33.0025

1807-3107-bor-33-e025.pdf - Published Version
Available under License Creative Commons: Attribution (CC-BY).

Download (2MB) | Preview

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.

Item Type:

Journal Article (Original Article)


04 Faculty of Medicine > School of Dental Medicine > Department of Periodontology
04 Faculty of Medicine > School of Dental Medicine > Periodontics Research

UniBE Contributor:

Eick, Sigrun


600 Technology > 610 Medicine & health




Sociedade Brasileira de Pesquisa Odontológica




Doris Burri

Date Deposited:

08 Jan 2020 10:03

Last Modified:

05 Dec 2022 15:35

Publisher DOI:


PubMed ID:





Actions (login required)

Edit item Edit item
Provide Feedback