International dental journal · 2025
METTL3-Mediated m6A Modification of DSC1 Alleviates Inflammation and Cellular Dysfunction in Periodontitis.
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.
Su Qin, Chen Jiao
Аннотация
BACKGROUND: The inflammation and cellular dysfunction in periodontitis largely depend on N6-methyladenosine (m6A) modification-related epigenetics. However, the role of methyltransferase-like 3 (METTL3)-differentiated m6A modification of desmocollin 1 (DSC1) in periodontitis remains to be investigated.
METHODS: Periodontal ligament (PDL) tissues were collected from patients with periodontitis and healthy volunteers, and a periodontitis model was constructed using lipopolysaccharide (LPS) and human periodontal ligament fibroblasts (HPLF). METTL3 and DSC1 levels in the specimens and cells were measured using quantitative reverse-transcription polymerase chain reaction. Proliferation, apoptosis, and inflammatory changes were analyzed using CCK-8, EdU, flow cytometry, and enzyme-linked immunosorbent assay, respectively. Additionally, m6A RNA immunoprecipitation was conducted to analyze the influence of METTL3 on the m6A modification of the DSC1 gene.
RESULTS: The expression levels of METTL3 and DSC1 were lower in patients with periodontitis compared to those in the healthy group. LPS treatment inhibited the survival of HPLF cells, promoting apoptosis and inflammation; alternatively, DSC1 overexpression alleviated the LPS-induced damage to periodontitis cells. Furthermore, METTL3 positively regulated the DSC1 level and enhanced its stability through m6A modification. Silencing METTL3 partially reversed the alleviating effect of DSC1 upregulation on inflammation and cellular dysfunction related to periodontitis in HPLF cells.
CONCLUSION: These findings suggest that METTL3 mediates the m6A modification of DSC1 to alleviate periodontitis-associated inflammation and cellular dysfunction.
METHODS: Periodontal ligament (PDL) tissues were collected from patients with periodontitis and healthy volunteers, and a periodontitis model was constructed using lipopolysaccharide (LPS) and human periodontal ligament fibroblasts (HPLF). METTL3 and DSC1 levels in the specimens and cells were measured using quantitative reverse-transcription polymerase chain reaction. Proliferation, apoptosis, and inflammatory changes were analyzed using CCK-8, EdU, flow cytometry, and enzyme-linked immunosorbent assay, respectively. Additionally, m6A RNA immunoprecipitation was conducted to analyze the influence of METTL3 on the m6A modification of the DSC1 gene.
RESULTS: The expression levels of METTL3 and DSC1 were lower in patients with periodontitis compared to those in the healthy group. LPS treatment inhibited the survival of HPLF cells, promoting apoptosis and inflammation; alternatively, DSC1 overexpression alleviated the LPS-induced damage to periodontitis cells. Furthermore, METTL3 positively regulated the DSC1 level and enhanced its stability through m6A modification. Silencing METTL3 partially reversed the alleviating effect of DSC1 upregulation on inflammation and cellular dysfunction related to periodontitis in HPLF cells.
CONCLUSION: These findings suggest that METTL3 mediates the m6A modification of DSC1 to alleviate periodontitis-associated inflammation and cellular dysfunction.