题名 | Tensile strength suppresses the osteogenesis of periodontal ligament cells in inflammatory microenvironments |
作者 | |
发表日期 | 2017-07 |
发表期刊 | MOLECULAR MEDICINE REPORTS 影响因子和分区 |
语种 | 英语 |
原始文献类型 | Article |
关键词 | periodontal ligament cell tensile strength cytokines osteogenesis interleukin-1 beta tumor necrosis factor-alpha |
其他关键词 | MESENCHYMAL STEM-CELLS ; TUMOR-NECROSIS-FACTOR ; ALKALINE-PHOSPHATASE ACTIVITY ; IN-VITRO ; GENE-EXPRESSION ; TNF-ALPHA ; MECHANICAL-STRESS ; GINGIVAL TISSUE ; DIFFERENTIATION ; INDUCTION |
摘要 | The present study aimed to investigate the role of orthodontic force in osteogenesis differentiation, matrix deposition and mineralization in periodontal ligament cells (PDLCs) cells in inflammatory microenvironments. The mesenchymal origin of PDLCs was confirmed by vimentin and cytokeratin staining. PDLCs were exposed to inflammatory cytokines (5 ng/ml IL-1 beta and 10 ng/ml TNF-alpha) and/or tensile strength (0.5 Hz, 12% elongation) for 12, 24 or 48 h. Cell proliferation and tensile strength-induced cytokine expression were assessed by MTT assay and ELISA, respectively. Runt-related transcription factor 2 (RUNX2) and type I collagen (COL-I) expression were analysed by reverse transcription-quantitative polymerase chain reaction and western blot analysis. Additionally, alkaline phosphatase activity was measured, and the mineralization profile was evaluated by alizarin red S staining. PDLCs exposed to tensile strength in inflammatory microenvironments exhibited reduced proliferation and mineralization potential. Treatment with the inflammatory cytokines IL-1 beta and TNF-alpha increased RUNX2 expression levels; however, decreased COL-I expression levels, indicating that bone formation and matrix deposition involve different mechanisms in PDL tissues. Notably, RUNX2 and COL-I expression levels were decreased in PDLCs exposed to a combination of an inflammatory environment and loading strength. The decreased osteogenic potential in an inflammatory microenvironment under tensile strength suggests that orthodontic force may amplify periodontal destruction in orthodontic patients with periodontitis. |
资助项目 | National Natural Science Foundation of China[2015KYA149]; |
出版者 | SPANDIDOS PUBL LTD |
出版地 | ATHENS |
ISSN | 1791-2997 |
EISSN | 1791-3004 |
卷号 | 16期号:1页码:666-672 |
DOI | 10.3892/mmr.2017.6644 |
页数 | 7 |
WOS类目 | Oncology ; Medicine, Research & Experimental |
WOS研究方向 | Oncology ; Research & Experimental Medicine |
WOS记录号 | WOS:000405074100088 |
收录类别 | SCIE ; PUBMED ; SCOPUS |
URL | 查看原文 |
PubMed ID | 28560407 |
PMC记录号 | PMC5482070 |
SCOPUSEID | 2-s2.0-85020715788 |
通讯作者地址 | [Deng, Hui]Department of Periodontics,School of Stomatology,Wenzhou Medical University,373 West Xueyuan Road,Wenzhou, Zhejiang,325027,China |
Scopus学科分类 | Biochemistry;Molecular Medicine;Molecular Biology;Genetics;Oncology;Cancer Research |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | https://kms.wmu.edu.cn/handle/3ETUA0LF/17567 |
专题 | 口腔医学院、附属口腔医院_口腔正畸 基础医学院(机能实验教学中心) |
通讯作者 | Deng, Hui |
作者单位 | 1.Department of Orthodontics,School of Stomatology,Wenzhou Medical University,373 West Xueyuan Road,Wenzhou, Zhejiang,325027,China; 2.Department of Histology and Embryology,School of Basic Medical Sciences,China; 3.Department of Periodontics,School of Stomatology,Wenzhou Medical University,373 West Xueyuan Road,Wenzhou, Zhejiang,325027,China; 4.Faculty of Dentistry,University of Hong Kong,Hong Kong,999077,Hong Kong |
第一作者单位 | 口腔医学院、附属口腔医院 |
通讯作者单位 | 口腔医学院、附属口腔医院 |
第一作者的第一单位 | 口腔医学院、附属口腔医院 |
推荐引用方式 GB/T 7714 | Sun, Chaofan,Liu, Fen,Cen, Shendan,et al. Tensile strength suppresses the osteogenesis of periodontal ligament cells in inflammatory microenvironments[J]. MOLECULAR MEDICINE REPORTS,2017,16(1):666-672. |
APA | Sun, Chaofan., Liu, Fen., Cen, Shendan., Chen, Lijiao., Wang, Yi., ... & Hu, Rongdang. (2017). Tensile strength suppresses the osteogenesis of periodontal ligament cells in inflammatory microenvironments. MOLECULAR MEDICINE REPORTS, 16(1), 666-672. |
MLA | Sun, Chaofan,et al."Tensile strength suppresses the osteogenesis of periodontal ligament cells in inflammatory microenvironments".MOLECULAR MEDICINE REPORTS 16.1(2017):666-672. |
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