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Updated: Jun 24, 2025

Inducing Apical Periodontitis in Mice
Published on: August 6, 2019
Long intergenic non-coding RNA 01126 activates IL-6/JAK2/STAT3 pathway to promote periodontitis pathogenesis
Song Tang1,2,3, Yi Zhong4, Jie Li1,2,3
1College of Stomatology, Chongqing Medical University, Chongqing, China.
Objectives:
Periodontitis seriously affects oral-related quality of life and overall health. Long intergenic non-coding RNA 01126 (LINC01126) is aberrantly expressed in periodontitis tissues. This study aimed to explore the possible pathogenesis of LINC01126 in periodontitis.
Methods:
Inflammatory model of human gingival fibroblasts (HGFs) was established. Cell Counting Kit-8 (CCK-8), wound healing assay, and flow cytometry were utilized to detect biological roles of LINC01126. Binding site of miR-655-3p to LINC01126 and IL-6 was predicted. Then, subcellular localization of LINC01126 and the binding ability of miR-655-3p to LINC01126 and IL-6 in HGFs were verified. Hematoxylin-Eosin (H&E) staining and immunohistochemistry (IHC) staining were utilized to detect tissue morphology and proteins expression of clinical samples.
Results:
LINC01126 silencing can alleviate cell inflammation induced by lipopolysaccharide derived from Porphyromonas gingivalis, reduce cell apoptosis, and promote cell migration. As a "sponge" for miR-655-3p, LINC01126 inhibits its binding to mRNA of IL-6, thereby promoting inflammation progression and JAK2/STAT3 pathway activation. Quantitative real-time PCR, Western Blot, and IHC results of clinical tissue samples further confirmed that miR-655-3p expression was down-regulated and IL-6/JAK2/STAT3 was abnormally activated in periodontitis tissues.
Conclusions:
In summary, serving as an endogenous competitive RNA of miR-655-3p, LINC01126 promotes IL-6/JAK2/STAT3 pathway activation, thereby promoting periodontitis pathogenesis.
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