Abstract
circRNA CDR1as (CDR1as) has been demonstrated to play important roles in a variety of inflammation-related diseases by acting as miRNA sponges. The present study is aimed at investigating the potential roles of CDR1as in the proliferation of human periodontal ligament stem cells (PDLSCs) under an inflammatory condition induced by Porphyromonas gingivalis-derived lipopolysaccharide (LPS). Human periodontal ligament cells (PDLCs) were isolated from periodontal ligament tissue, and PDLSCs were sorted from PDLCs based on the STRO-1 expression through fluorescence-activated cell sorting. We further found that CDR1as was significantly downregulated in LPS-treated PDLSCs compared to untreated cells, as well as in normal periodontal ligament tissues compared to periodontitis tissues. Knockdown of CDR1as promoted LPS-induced proliferative inhibition of PDLSCs, whereas overexpression of CDR1as alleviated the LPS-induced proliferative ability of PDLSCs. Mechanistically, CDR1as functioned as an miR-7 sponge to activate the ERK signal pathway to mediate the inhibition effect of LPS on cell proliferation. Taken together, our findings revealed the effects of the interacting pair of CDR1as/miR-7 on the proliferation ability of PDLSCs within their surrounding inflammatory microenvironment of periodontitis.
Highlights
Periodontitis is the most prevalent chronic inflammatory disease in the tooth-supporting tissues caused by the accumulation of subgingival plaque and the action of specific periodontopathogenic bacteria [1]
We investigated the role of circRNA CDR1as (CDR1as) in the proliferation of Periodontal ligament stem cells (PDLSCs), as well as the mechanisms involved, under an inflammatory condition induced by P gingivalisderived LPS, the major component of the outer membrane of gram-negative bacteria and a pertinent deleterious factor in the oral microenvironment
CircRNA CDR1as was demonstrated to regulate the proliferation under a LPS-induced inflammatory condition by sponging miR-7 to activate the ERK signal pathway
Summary
Periodontitis is the most prevalent chronic inflammatory disease in the tooth-supporting tissues caused by the accumulation of subgingival plaque and the action of specific periodontopathogenic bacteria [1]. Porphyromonas gingivalis (P. gingivalis) is one of the main bacteria associated with chronic periodontitis [2]. Periodontal tissue regeneration has close relationships with abilities of cell proliferation, migration, and osteo/dentinogenic differentiation of MSCs in an inflammatory niche [7]. In performing their periodontal tissue regenerative activity when inflammation is regarded as the reason for tissue damage, PDLSCs interact with their surrounding inflammatory microenvironment
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