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

Yajie Wu1, Zhifei Su2, Bowen Zhang3

  • 1State Key Laboratory of Oral Diseases, National Center for Stomatology, and National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China; Department of Endodontics, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, China.

Archives of Oral Biology
|October 10, 2025
PubMed
Abstract

Insights

Long noncoding RNA Mirt2 plays a key role in inflammatory bone loss. Mirt2 may be a potential therapeutic target for treating chronic inflammation-related bone loss diseases.

Area of Science:

  • Molecular Biology
  • Genetics
  • Immunology

Background:

  • Long noncoding RNAs (lncRNAs) are involved in various inflammatory diseases.
  • Myocardial infarction-associated transcript 2 (Mirt2) is an lncRNA with a known role in inflammation.
  • Inflammatory alveolar bone loss is a significant clinical concern.

Purpose of the Study:

  • To investigate the functional mechanism of Mirt2 in inflammatory alveolar bone loss.
  • To explore Mirt2 as a potential therapeutic target for inflammation-related bone loss.

Main Methods:

  • Utilized mouse models of periodontitis and periapical periodontitis.
  • Employed micro-CT and quantitative PCR (qPCR) to assess Mirt2 expression and role.
  • Conducted fluorescence in situ hybridization (FISH), ELISA, and alkaline phosphatase staining to confirm Mirt2 function.

Main Results:

  • Mirt2 expression was significantly elevated in inflammatory alveolar bone diseases.
  • LPS stimulation increased Mirt2 expression in MC3T3-E1 cells, with Mirt2 localized in the cytoplasm.
  • Mirt2 knockdown worsened LPS-induced inflammation, while Mirt2 overexpression attenuated inflammation and improved osteogenic differentiation.

Conclusions:

  • lncRNA Mirt2 demonstrates a significant role in chronic inflammation-associated bone loss.
  • Mirt2 presents a promising therapeutic target for future investigations into treating inflammation-related bone loss.