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Abstract 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.
Tang et al. (Sun,) studied this question.