Mirt2 alleviates LPS-induced inflammation of osteoblasts in alveolar bone destruction.

Abstract

OBJECTIVES: The long noncoding RNA (lncRNA) myocardial infarction-associated transcript 2 (Mirt2) has been confirmed to affect several inflammatory diseases. This study was conducted to explore the functional mechanism of Mirt2 in inflammatory alveolar bone loss and its possibility of being a therapeutic target. DESIGN: The expression level and potential role of Mirt2 in chronic inflammatory alveolar bone loss in mouse models of periodontitis and periapical periodontitis were investigated using micro-CT and qPCR. The characteristics of Mirt2 were evaluated by FISH, qPCR, ELISA, and alkaline phosphatase staining to confirm its function and mechanism of action in inflammatory response. RESULTS: Mirt2 expression was significantly enriched in inflammatory alveolar bone diseases. Mirt2 expression increased upon LPS stimulation in MC3T3-E1 cells (P&#x202f;<&#x202f;0.05), located at the cell cytoplasm. Mirt2 knockdown exacerbated the LPS-stimulated inflammatory response in MC3T3-E1 cells, whereas Mirt2 overexpression attenuated this effect and rescued LPS-impaired osteogenic differentiation. CONCLUSIONS: lncRNA Mirt2 suggests a potential role in chronic inflammation-related bone loss, providing potential therapeutic target worthy of future investigation for inflammation-related bone loss.