Calcium ions released from mineral trioxide aggregate convert the differentiation pathway of C2C12 cells into osteoblast lineage.
Matsumoto S., Hayashi M., Suzuki Y., Suzuki N., Maeno M., Ogiso B.
Laboratory Study, published in J Endod (2012) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- J Endod (2012)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 23228260
- DOI
- 10.1016/j.joen.2012.10.006
Abstract (original English)
The purpose of this study was to examine the effect of mineral trioxide aggregate (MTA) on pluripotent-mesenchymal cell differentiation. The pluripotent-mesenchymal cell line C2C12 was cultured in a 5% serum medium to induce cell differentiation with or without MTA. The differentiation to myoblasts was analyzed by the immunocytochemical staining of myosin heavy chains. The cellular phenotype-specific markers characterizing the osteoblasts (Runx2 and osterix), chondroblasts (Sox9), myoblasts (MyoD), and adipocytes (LPL) were estimated with mRNA and protein levels by using real-time polymerase chain reaction and Western blot analysis, respectively. To verify that the effect of MTA was caused by the released calcium ions, the mRNA levels were analyzed in the presence or absence of MTA with ethylene glycol tetraacetic acid, calcium chloride, or verapamil. C2C12 cells cultured without MTA altered their phenotype to myoblasts, exhibiting positive reactions to myosin heavy chains. However, the cells cultured with MTA were strongly inhibited from developing into myoblasts. The mRNA and protein expressions of Runx2, osterix, and Sox9 significantly increased with MTA; the expressions of MyoD and LPL decreased significantly. Calcium chloride addition without MTA presented a significant increase of mRNA levels of Runx2, osterix, and Sox9; ethylene glycol tetraacetic acid addition with MTA
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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