Irisin promotes cementoblast differentiation via p38 MAPK pathway.
Jiaqi Zhu1, Yunlong Wang1, Zhengguo Cao1
1The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China.
Oral Diseases
|February 19, 2020
Summary
Irisin, an exercise-induced myokine, promotes cementoblast differentiation and mineralization. This process is mediated through the p38 MAPK pathway, influencing bone health.
Area of Science:
- Biochemistry
- Cell Biology
- Endocrinology
Background:
- Irisin is an exercise-induced myokine impacting glucose metabolism and bone health.
- The role of irisin in cementoblast function, crucial for tooth root development and repair, is not well understood.
Purpose of the Study:
- To investigate the effect of irisin on cementoblast differentiation and mineralization.
- To elucidate the underlying molecular mechanisms, particularly the involvement of the p38 MAPK pathway.
Main Methods:
- Utilized an immortalized mouse cementoblast cell line (OCCM-30).
- Assessed cementoblast differentiation markers (Runx2, osterix, ALP, osteocalcin) and PGC-1α expression via qRT-PCR and Western blot.
- Evaluated mineralization using alizarin red staining.
- Investigated the p38 MAPK pathway using inhibitor SB203580 and siRNA.
- Examined cell proliferation with the CCK-8 assay.
Main Results:
- Irisin significantly increased cementoblast differentiation markers and mineralized nodule formation.
- Irisin upregulated the activity of the p38 MAPK pathway.
- Inhibition of the p38 MAPK pathway suppressed irisin-induced cementoblast differentiation.
- High-dose irisin treatment enhanced OCCM-30 cell proliferation over extended periods.
Conclusions:
- Irisin promotes cementoblast differentiation and mineralization.
- The p38 MAPK pathway is essential for mediating irisin's effects on cementoblasts.
- Irisin may play a role in regulating cementum formation and repair.
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