Circ_0036490 and DKK1 competitively bind miR-29a to promote lipopolysaccharides-induced human gingival fibroblasts injury

MicroRNA (miRNA) plays a regulatory role in periodontitis. This study aimed to explore whether miR-29a could affect lipopolysaccharides (LPSs)-induced injury in human gingival fibroblasts (HGFs) through the competitive endogenous RNAs (ceRNA) mechanism. Periodontal ligament (PDL) tissues and HGFs we...

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Main Authors: Yeke Wu, Bin Li, Disi Deng, Hongling Zhou, Min Liu, Huangping Ai, Yilin Xin, Weihan Hua, Lixing Zhao, Li Li
Format: Article
Language:English
Published: Taylor & Francis Group 2024-12-01
Series:Autoimmunity
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Online Access:https://www.tandfonline.com/doi/10.1080/08916934.2024.2312927
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author Yeke Wu
Bin Li
Disi Deng
Hongling Zhou
Min Liu
Huangping Ai
Yilin Xin
Weihan Hua
Lixing Zhao
Li Li
author_facet Yeke Wu
Bin Li
Disi Deng
Hongling Zhou
Min Liu
Huangping Ai
Yilin Xin
Weihan Hua
Lixing Zhao
Li Li
author_sort Yeke Wu
collection DOAJ
description MicroRNA (miRNA) plays a regulatory role in periodontitis. This study aimed to explore whether miR-29a could affect lipopolysaccharides (LPSs)-induced injury in human gingival fibroblasts (HGFs) through the competitive endogenous RNAs (ceRNA) mechanism. Periodontal ligament (PDL) tissues and HGFs were derived from patients with periodontitis and healthy volunteers. Periodontitis cell model was established by treating HGFs with LPS. Expression levels of circ_0036490, miR-29a, and DKK1 were evaluated by the reverse transcription quantitative real-time PCR (RT-qPCR) method. Western blotting assay was performed to assess protein expression levels of pyroptosis-related proteins and Wnt signalling related proteins. Cell viability was evaluated by cell counting kit-8 (CCK-8) assay. Concentration of lactate dehydrogenase (LDH), interleukin (IL)-1β, and IL-18 were determined by Enzyme-linked immunosorbent assay (ELISA). Pyroptosis rate were determined by flow cytometry assay to evaluate pyroptosis. The interaction between miR-29a and circ_0036490 or DKK1 was verified by dual-luciferase reporter and RNA pull-down assays. MiR-29a expression was lower in PDL tissues of patients with periodontitis than that in healthy group; likewise, miR-29a was also downregulated in LPS-treated HGFs. Overexpression of miR-29a increased cell viability and decreased pyroptosis of HGFs induced by LPS while inhibition of miR-29a exerted the opposite role. MiR-29a binds to circ_0036490 and elevation of circ_0036490 contributed to dysfuntion of LPS-treated HGFs and reversed the protection function of elevated miR-29a. In addition, miR-29a targets DKK1. Overexpression of DKK1 abrogated the effects of overexpressed miR-29a on cell vaibility, pyroptosis, and protein levels of Wnt signalling pathway of LPS-treated HGFs. Circ_0036490 and DKK1 competitively bind miR-29a to promote LPS-induced HGF injury in vitro. Wnt pathway inactivated by LPS was activated by miR-29a. Thence, miR-29a may be a promising target for periodontitis.
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series Autoimmunity
spelling doaj-art-a73a0ce5fec241dcb97dbb252ecd70f12025-08-20T02:38:31ZengTaylor & Francis GroupAutoimmunity0891-69341607-842X2024-12-0157110.1080/08916934.2024.2312927Circ_0036490 and DKK1 competitively bind miR-29a to promote lipopolysaccharides-induced human gingival fibroblasts injuryYeke Wu0Bin Li1Disi Deng2Hongling Zhou3Min Liu4Huangping Ai5Yilin Xin6Weihan Hua7Lixing Zhao8Li Li9Department of Stomatology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, ChinaDepartment of Geriatrics, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, ChinaCollege of Clinical Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, ChinaState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of Orthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, ChinaCollege of Clinical Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, ChinaCollege of Clinical Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, ChinaState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of Orthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, ChinaState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of Orthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, ChinaState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of Orthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, ChinaDepartment of Radiology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, ChinaMicroRNA (miRNA) plays a regulatory role in periodontitis. This study aimed to explore whether miR-29a could affect lipopolysaccharides (LPSs)-induced injury in human gingival fibroblasts (HGFs) through the competitive endogenous RNAs (ceRNA) mechanism. Periodontal ligament (PDL) tissues and HGFs were derived from patients with periodontitis and healthy volunteers. Periodontitis cell model was established by treating HGFs with LPS. Expression levels of circ_0036490, miR-29a, and DKK1 were evaluated by the reverse transcription quantitative real-time PCR (RT-qPCR) method. Western blotting assay was performed to assess protein expression levels of pyroptosis-related proteins and Wnt signalling related proteins. Cell viability was evaluated by cell counting kit-8 (CCK-8) assay. Concentration of lactate dehydrogenase (LDH), interleukin (IL)-1β, and IL-18 were determined by Enzyme-linked immunosorbent assay (ELISA). Pyroptosis rate were determined by flow cytometry assay to evaluate pyroptosis. The interaction between miR-29a and circ_0036490 or DKK1 was verified by dual-luciferase reporter and RNA pull-down assays. MiR-29a expression was lower in PDL tissues of patients with periodontitis than that in healthy group; likewise, miR-29a was also downregulated in LPS-treated HGFs. Overexpression of miR-29a increased cell viability and decreased pyroptosis of HGFs induced by LPS while inhibition of miR-29a exerted the opposite role. MiR-29a binds to circ_0036490 and elevation of circ_0036490 contributed to dysfuntion of LPS-treated HGFs and reversed the protection function of elevated miR-29a. In addition, miR-29a targets DKK1. Overexpression of DKK1 abrogated the effects of overexpressed miR-29a on cell vaibility, pyroptosis, and protein levels of Wnt signalling pathway of LPS-treated HGFs. Circ_0036490 and DKK1 competitively bind miR-29a to promote LPS-induced HGF injury in vitro. Wnt pathway inactivated by LPS was activated by miR-29a. Thence, miR-29a may be a promising target for periodontitis.https://www.tandfonline.com/doi/10.1080/08916934.2024.2312927Periodontitishuman gingival fibroblastspyroptosiscirc_0036490miR-29aDKK1
spellingShingle Yeke Wu
Bin Li
Disi Deng
Hongling Zhou
Min Liu
Huangping Ai
Yilin Xin
Weihan Hua
Lixing Zhao
Li Li
Circ_0036490 and DKK1 competitively bind miR-29a to promote lipopolysaccharides-induced human gingival fibroblasts injury
Autoimmunity
Periodontitis
human gingival fibroblasts
pyroptosis
circ_0036490
miR-29a
DKK1
title Circ_0036490 and DKK1 competitively bind miR-29a to promote lipopolysaccharides-induced human gingival fibroblasts injury
title_full Circ_0036490 and DKK1 competitively bind miR-29a to promote lipopolysaccharides-induced human gingival fibroblasts injury
title_fullStr Circ_0036490 and DKK1 competitively bind miR-29a to promote lipopolysaccharides-induced human gingival fibroblasts injury
title_full_unstemmed Circ_0036490 and DKK1 competitively bind miR-29a to promote lipopolysaccharides-induced human gingival fibroblasts injury
title_short Circ_0036490 and DKK1 competitively bind miR-29a to promote lipopolysaccharides-induced human gingival fibroblasts injury
title_sort circ 0036490 and dkk1 competitively bind mir 29a to promote lipopolysaccharides induced human gingival fibroblasts injury
topic Periodontitis
human gingival fibroblasts
pyroptosis
circ_0036490
miR-29a
DKK1
url https://www.tandfonline.com/doi/10.1080/08916934.2024.2312927
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