TNF-α Directly Enhances Osteocyte RANKL Expression and Promotes Osteoclast Formation.
Animals
Biomarkers
Biopsy
Cells, Cultured
Coculture Techniques
Gene Expression Regulation
Immunophenotyping
MAP Kinase Signaling System
Mice
Osteoclasts
/ metabolism
Osteocytes
/ metabolism
Osteogenesis
RANK Ligand
/ genetics
Receptors, Tumor Necrosis Factor, Type I
/ genetics
Receptors, Tumor Necrosis Factor, Type II
/ genetics
Tumor Necrosis Factor-alpha
/ metabolism
RANKL
TNF-α
osteoclastogenesis
osteocyte
osteoimmunology
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2019
2019
Historique:
received:
15
08
2019
accepted:
28
11
2019
entrez:
11
1
2020
pubmed:
11
1
2020
medline:
11
11
2020
Statut:
epublish
Résumé
Osteoimmunology peeks into the interaction of bone and the immune system, which has largely proved to be a multiplex reaction. Osteocytes have been shown to regulate bone resorption through the expression of RANKL in physiologic and pathologic conditions. TNF-α, a product of the immune system, is an important cytokine regulating bone resorption in inflammatory conditions either directly or by increasing RANKL and M-CSF expressions by osteoblasts and stromal cells. The effect of TNF-α on a wide range of cell types has been documented; however, the direct effect of TNF-α on osteocytes has not been established yet. In this study, primary osteocytes were isolated by cell sorting from neonatal calvaria of Dmp1-Topaz mice, which express the green fluorescent protein under the influence of dentin matrix protein 1 promoter. The results show that osteocytes have a significantly higher RANKL mRNA expression when cultured with TNF-α. A co-culture system of osteocytes and TNF receptors I and II deficient osteoclast precursors treated with TNF-α show a significant increase in TRAP-positive cells while cultures without TNF-α failed to show TRAP-positive cells. Additionally,
Identifiants
pubmed: 31921183
doi: 10.3389/fimmu.2019.02925
pmc: PMC6923682
doi:
Substances chimiques
Biomarkers
0
RANK Ligand
0
Receptors, Tumor Necrosis Factor, Type I
0
Receptors, Tumor Necrosis Factor, Type II
0
Tnfrsf1a protein, mouse
0
Tnfrsf1b protein, mouse
0
Tumor Necrosis Factor-alpha
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2925Informations de copyright
Copyright © 2019 Marahleh, Kitaura, Ohori, Kishikawa, Ogawa, Shen, Qi, Noguchi, Nara and Mizoguchi.
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