Archives of oral biology · 2025
Mirt2 alleviates LPS-induced inflammation of osteoblasts in alveolar bone destruction.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wu Yajie, Su Zhifei, Zhang Bowen, Cheng Lei, Wang Ziyou, Yuan He, Li Jiyao
Аннотация
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 < 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.
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 < 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.