Each odontoblast is tightly linked to other odontoblasts. They form a line of defense and are capable of withstanding external stimuli, particularly the inflammation caused by caries. Thus, we investigated exosomes derived from odontoblasts as an intercellular mechanism by which inflamed odontoblasts are protected from apoptosis. CD63, an exosome marker, was expressed at high levels in caries-affected regions of the dental pulp. We conducted an ex vivo experiment by applying different concentrations of lipopolysaccharide (LPS) to the odontoblast-like cells (mineralization was induced in stem cells derived from the apical papilla). Odontoblast-like cells treated with a high concentration of LPS (20 µg/mL LPS, severely affected) exhibited an accelerated release of exosomes, which attenuated the LPS-induced cell apoptosis of odontoblast-like cells treated with a low concentration of LPS (1 µg/mL LPS, mildly affected). Next, we blocked exosome uptake with chlorpromazine, and the rescue effect vanished. Based on our findings, severely inflamed odontoblasts attenuate the apoptosis of mildly inflamed neighboring cells through an exosome-mediated intercellular signaling pathway.
These authors contributed equally to this work. REFERENCES 1 Proud CG. The multifaceted role of mTOR in cellular stress responses. DNA Repair (Amst) 2004; 3: 927-934. 2 Foster KG, Fingar DC. Mammalian target of rapamycin (mTOR): conducting the cellular signaling symphony.
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