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Войти в исследования Journal of clinical periodontology · 2022
Long non-coding RNA SNHG5 mediates periodontal inflammation through the NF-κB signalling pathway.
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Han Yineng, Huang Yiping, Yang Qiaolin, Jia Lingfei, Zheng Yunfei, Li Weiran
Аннотация
AIM: We investigated the role of long non-coding RNAs and small nucleolar RNA host gene 5 (SNHG5) in the pathogenesis of periodontitis.
MATERIALS AND METHODS: A ligature-induced periodontitis mouse model was established, and gingival tissues were collected from patients with periodontitis and healthy controls. Inflammatory cytokines were detected using quantitative reverse transcription-polymerase chain reaction and western blotting analyses. Direct interactions between SNHG5 and p65 were detected by RNA pull-down and RNA immunoprecipitation assays. Micro-computed tomography, haematoxylin and eosin staining, and immunohistochemical staining were used to measure periodontal bone loss.
RESULTS: SNHG5 expression was down-regulated in human and mouse periodontal tissues compared to that in the healthy controls. In vitro experiments demonstrated that SNHG5 significantly ameliorated tumour necrosis factor α-induced inflammation. Mechanistically, SNHG5 directly binds to the nuclear factor-kappa B (NF-κB) p65 subunit and inhibits its translocation, thereby suppressing the NF-κB signalling pathway activation and reducing the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing three inflammasome expression. Locally injecting si-SNHG5 aggravated the periodontal destruction.
CONCLUSION: This study revealed that SNHG5 mediates periodontal inflammation through the NF-κB signalling pathway, providing a potential therapeutic target for periodontitis treatment.
MATERIALS AND METHODS: A ligature-induced periodontitis mouse model was established, and gingival tissues were collected from patients with periodontitis and healthy controls. Inflammatory cytokines were detected using quantitative reverse transcription-polymerase chain reaction and western blotting analyses. Direct interactions between SNHG5 and p65 were detected by RNA pull-down and RNA immunoprecipitation assays. Micro-computed tomography, haematoxylin and eosin staining, and immunohistochemical staining were used to measure periodontal bone loss.
RESULTS: SNHG5 expression was down-regulated in human and mouse periodontal tissues compared to that in the healthy controls. In vitro experiments demonstrated that SNHG5 significantly ameliorated tumour necrosis factor α-induced inflammation. Mechanistically, SNHG5 directly binds to the nuclear factor-kappa B (NF-κB) p65 subunit and inhibits its translocation, thereby suppressing the NF-κB signalling pathway activation and reducing the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing three inflammasome expression. Locally injecting si-SNHG5 aggravated the periodontal destruction.
CONCLUSION: This study revealed that SNHG5 mediates periodontal inflammation through the NF-κB signalling pathway, providing a potential therapeutic target for periodontitis treatment.