Effect of Oxidative Stress-Induced Apoptosis on Active FGF23 Levels in MLO-Y4 Cells: The Protective Role of 17-β-Estradiol.
Adaptor Proteins, Signal Transducing
/ metabolism
Animals
Apoptosis
/ drug effects
Bone Remodeling
/ drug effects
Bone and Bones
/ drug effects
Cell Line
Down-Regulation
/ drug effects
Estradiol
/ pharmacology
Estrogens
/ metabolism
Fibroblast Growth Factor-23
/ metabolism
Gene Expression Regulation
/ drug effects
Mice
Osteocytes
/ drug effects
Osteogenesis
/ drug effects
Oxidative Stress
/ drug effects
Protective Agents
/ pharmacology
Signal Transduction
/ drug effects
Up-Regulation
/ drug effects
FGF23
estrogen
oxidative stress-induced apoptosis
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
14 Feb 2022
14 Feb 2022
Historique:
received:
31
01
2022
revised:
10
02
2022
accepted:
11
02
2022
entrez:
26
2
2022
pubmed:
27
2
2022
medline:
15
3
2022
Statut:
epublish
Résumé
The discovery that osteocytes secrete phosphaturic fibroblast growth factor 23 (FGF23) has defined bone as an endocrine organ. However, the autocrine and paracrine functions of FGF23 are still unknown. The present study focuses on the cellular and molecular mechanisms involved in the complex control of FGF23 production and local bone remodeling functions. FGF23 was assayed using ELISA kit in the presence or absence of 17β-estradiol in starved MLO-Y4 osteocytes. In these cells, a relationship between oxidative stress-induced apoptosis and up-regulation of active FGF23 levels due to MAP Kinases activation with involvement of the transcriptional factor (NF-kB) has been demonstrated. The active FGF23 increase can be due to up-regulation of its expression and post-transcriptional modifications. 17β-estradiol prevents the increase of FGF23 by inhibiting JNK and NF-kB activation, osteocyte apoptosis and by the down-regulation of osteoclastogenic factors, such as sclerostin. No alteration in the levels of dentin matrix protein 1, a FGF23 negative regulator, has been determined. The results of this study identify biological targets on which drugs and estrogen may act to control active FGF23 levels in oxidative stress-related bone and non-bone inflammatory diseases.
Identifiants
pubmed: 35216216
pii: ijms23042103
doi: 10.3390/ijms23042103
pmc: PMC8879671
pii:
doi:
Substances chimiques
Adaptor Proteins, Signal Transducing
0
Estrogens
0
Fgf23 protein, mouse
0
Protective Agents
0
Estradiol
4TI98Z838E
Fibroblast Growth Factor-23
7Q7P4S7RRE
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
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