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Updated: Jan 28, 2026

Isolation of Mesenchymal Stem Cells from Human Alveolar Periosteum and Effects of Vitamin D on Osteogenic Activity of Periosteum-derived Cells
Published on: May 4, 2018
FGF23 and Fetuin-A Interaction and Mesenchymal Osteogenic Transformation
Deborah Mattinzoli1, Masami Ikehata2, Koji Tsugawa3
1Renal Research Laboratory Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy. deborah.mattinzoli@policlinico.mi.it.
Mesenchymal stem cells produce Fibroblast growth factor 23 (FGF23), which drives Fetuin-A production. This FGF23-Fetuin-A interaction in bone marrow suggests a role in osteoblast differentiation and mineral bone disorders.
Area of Science:
- Cell Biology
- Endocrinology
- Bone Biology
Background:
- Fibroblast growth factor 23 (FGF23) and Fetuin-A are linked in cardiovascular and mineral bone disorders.
- Bone marrow positivity for both FGF23 and Fetuin-A was previously uninvestigated.
- The production of FGF23 by mesenchymal stem cells (MSCs) was unknown.
Purpose of the Study:
- To investigate FGF23 production by MSCs.
- To elucidate the regulatory relationship between FGF23 and Fetuin-A within MSCs.
- To explore the role of FGF23 and Fetuin-A in osteoblast differentiation.
Main Methods:
- Immunostaining, qRT-PCR, ELISA, chromatin immunoprecipitation, and transfection were used.
- Duolink proximity ligation assay assessed FGF23-Fetuin-A interaction.
- Human primary cells and mouse/human cell lines were studied.
Main Results:
- MSCs produce FGF23, with expression increasing during osteo-differentiation.
- FGF23 directly binds to the Fetuin-A promoter, activating its transcription.
- FGF23 overexpression/addition upregulated Fetuin-A, an effect dependent on FGF23.
Conclusions:
- FGF23 and Fetuin-A are present and interact within MSCs.
- FGF23 drives Fetuin-A production in MSCs.
- This mechanism suggests a role for FGF23 and Fetuin-A in osteoblast differentiation.
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