Abstract

Background/purposeIt was reported that lncRNAs have an effect on immune-related diseases, however, their roles in periodontitis remain to be investigated. The aim of this study was to look for immune-related lncRNAs in periodontitis, and to preliminarily explore their function in vitro. Materials and methodsCIBERSORT was used to analyze abundance of immune cell in the periodontal tissue. Correlation between the expression profile of lncRNAs and abundance of immune cell was calculated and immune-related lncRNAs were identified. The expressions of immune-related lncRNAs identified were validated by RT-qPCR with 15 periodontitis and 15 healthy gingival tissues. The expressions of PRKCQ-AS1 and EGOT in HGFs were detected under the stimulation of different concentrations of TNF-α (0, 10, 15, 20, 30 ng/mL) and different duration (0, 12, 24 and 48 h). Then, siRNA was used to silence PRKCQ-AS1 and EGOT in HGFs. The expression level of IL-1β, IL-6, IL-8 of the HGFs after stimulated by 15 ng/mL TNF-α, and the activation of NF-κB pathway was observed. ResultsPRKCQ-AS1 and EGOT were identified as top 2 immune-related lncRNAs in periodontal tissues. The expressions of PRKCQ-AS1 and EGOT were significantly up-regulated in inflamed periodontal tissue and in HGFs under TNF-α stimulation. After knock-down of PRKCQ-AS1 and EGOT, expression level of IL-1β, IL-6, and IL-8 in HGFs with TNF-α stimulation were decreased, and activation of NF-κB pathway was inhibited. ConclusionPRKCQ-AS1 and EGOT were firstly identified as immune-related lncRNAs in periodontal tissue, and they regulate the expression of IL-1β, IL-6, and IL-8 of HGFs through the NF-κB pathway.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.