Abnormal expression of long noncoding RNA FGD5-AS1 affects the development of periodontitis through regulating miR-142-3p/SOCS6/NF-κB pathway

Abstract

Periodontitis refers to the inflammation of gums and the surrounding structures and caused by a bacterial infection. The infection occurs owing to poor oral hygiene and could destroy the bone and the gum over time if left untreated. The present study identified the involvement of a key long noncoding RNA (lncRNA), i.e. FGD5-AS1, in the pathogenesis of periodontitis by assessing its expression in the gingival tissues of patients diagnosed with chronic periodontitis (CP). Overexpression of FGD5-AS1 in primary human periodontal ligament cells (PDLCs) significantly reduced the lipopolysaccharide (LPS)induced periodontitis, whereas its suppression aggravated this injury. Moreover, the miR-142-3p was markedly expressed in the gingival samples of patients diagnosed with CP and LPS-induced PDLCs. We found that the FGD5-AS1-mediated reduction in the inflammation was mediated through downside regulation of miR-142-3p, as evident from the upregulation of SOCS6, a target gene of miR-142-3p. Furthermore, the association between FGD5-AS1 and NF-jB pathway was detected. FGD5-AS1 was found to protect against LPS-stimulated PDLC injury through restraining the NF-jB signals. Based on these findings, we conclude that up-regulation of lncRNA FGD5-AS1 could protect against periodontitis via regulating the miR-142-3p/SOCS6/NF-jB signals. Therefore, the FGD5-AS1/miR-142-3p/SOCS6 axis may act as an important indicator in explaining the pathogenesis of periodontitis.

Expression of MicroRNAs in Periodontal and Peri-Implant Diseases: A Systematic Review and Meta-Analysis

“…Among all 43 included articles, a total of 563 miRNAs were identified reporting fold changes in miRNA expression between health and periodontal/peri-implant disease (Tables S9 and S10). Due to extensiveness and limitations in the reported data, only 16 miRNAs were selected to perform a meta-analysis and were chosen if fold changes values of the same miRNA were reported in both animal and human studies or individually, in more than two and four articles from animal and human studies, respectively [13,15,17,18,[20][21][22][23]26,28,29,[31][32][33]35,37,38,41,42,[44][45][46][47][48][49][50][51].…”

Regulation of the miR-19b-mediated SOCS6-JAK2/STAT3 pathway by lncRNA MEG3 is involved in high glucose-induced apoptosis in hRMECs

“…As reported, up-regulation of SOCS3 inhibited MMP-9 expression in retinal microglia induced by high glucose [26]. According to Chen's study, SOCS6 was identified as the target of miR-142-3p in primary human periodontal ligament cells [27]. In addition, SOCS6 was considered a negative regulator of cytokine receptor signalling.…”

lncRNA FGD5 antisense RNA 1 upregulates RORA to suppress hypoxic injury of human cardiomyocyte cells by inhibiting oxidative stress and apoptosis via miR‑195

“…These outcomes indicated a suppressive effect of FGd5-aS1 in hypoxia-induced oxidative injury of cardiomyocytes. chen et al (28) reported a protective role of FGd5-aS1 in lipopolysaccharide-induced inflammatory injury in human periodontal ligament cells, as evidenced by counteraction of cell apoptosis and pro-inflammatory cytokine secretion via the nF-κB pathway. The role of FGD5-AS1 in inflammation in AMI requires further investigation, although ischemia-hypoxia is known to highly induce an inflammatory response in AMI (29).…”