circRNA CDR1as Regulated the Proliferation of Human Periodontal Ligament Stem Cells under a Lipopolysaccharide-Induced Inflammatory Condition
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 in...
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| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2019-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2019/1625381 |
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| _version_ | 1832559458709929984 |
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| author | Fang Wang Xi Chen Ying Han Shuang Xi Guofeng Wu |
| author_facet | Fang Wang Xi Chen Ying Han Shuang Xi Guofeng Wu |
| author_sort | Fang Wang |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-f6b85bba033241829bb064aaa5419634 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2019-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-f6b85bba033241829bb064aaa54196342025-02-03T01:30:06ZengWileyMediators of Inflammation0962-93511466-18612019-01-01201910.1155/2019/16253811625381circRNA CDR1as Regulated the Proliferation of Human Periodontal Ligament Stem Cells under a Lipopolysaccharide-Induced Inflammatory ConditionFang Wang0Xi Chen1Ying Han2Shuang Xi3Guofeng Wu4Key laboratory of Shaanxi Province for Craniofacial Precision Medicine Research & Department of Prosthodontics, College of Stomatology, Xi’an Jiaotong University, Xi’an, Shaanxi, ChinaDepartment of Prosthodontics, Digital Stomatological Engineering Center, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, ChinaKey laboratory of Shaanxi Province for Craniofacial Precision Medicine Research & Department of Prosthodontics, College of Stomatology, Xi’an Jiaotong University, Xi’an, Shaanxi, ChinaKey laboratory of Shaanxi Province for Craniofacial Precision Medicine Research & Department of Prosthodontics, College of Stomatology, Xi’an Jiaotong University, Xi’an, Shaanxi, ChinaDepartment of Prosthodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, Jiangsu, ChinacircRNA 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.http://dx.doi.org/10.1155/2019/1625381 |
| spellingShingle | Fang Wang Xi Chen Ying Han Shuang Xi Guofeng Wu circRNA CDR1as Regulated the Proliferation of Human Periodontal Ligament Stem Cells under a Lipopolysaccharide-Induced Inflammatory Condition Mediators of Inflammation |
| title | circRNA CDR1as Regulated the Proliferation of Human Periodontal Ligament Stem Cells under a Lipopolysaccharide-Induced Inflammatory Condition |
| title_full | circRNA CDR1as Regulated the Proliferation of Human Periodontal Ligament Stem Cells under a Lipopolysaccharide-Induced Inflammatory Condition |
| title_fullStr | circRNA CDR1as Regulated the Proliferation of Human Periodontal Ligament Stem Cells under a Lipopolysaccharide-Induced Inflammatory Condition |
| title_full_unstemmed | circRNA CDR1as Regulated the Proliferation of Human Periodontal Ligament Stem Cells under a Lipopolysaccharide-Induced Inflammatory Condition |
| title_short | circRNA CDR1as Regulated the Proliferation of Human Periodontal Ligament Stem Cells under a Lipopolysaccharide-Induced Inflammatory Condition |
| title_sort | circrna cdr1as regulated the proliferation of human periodontal ligament stem cells under a lipopolysaccharide induced inflammatory condition |
| url | http://dx.doi.org/10.1155/2019/1625381 |
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