{"title":"Concentrate Growth Factors Regulate Osteogenic Dysfunction of MC3T3-E1 Cells Induced by High Glucose Through PI3K/Akt Signaling Pathway.","authors":"Kai Dong, Pengjie Hao, Wenjuan Zhou, Zhonghao Liu","doi":"10.1097/ID.0000000000000921","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>The aim of this study is to investigate the effects of Concentrate Growth Factors Extract (CGF-e) on the proliferation and osteogenic differentiation of MC3T3-E1 cells under high glucose condition.</p><p><strong>Materials and methods: </strong>MC3T3-E1 cells were divided into 4 groups including normal glucose (5.5-mM) group (control), high glucose (25.5-mM) group, normal glucose + CGF-e group, and high glucose + CGF-e group. The proliferation, osteogenic differentiation and mineralization of osteoblasts were evaluated, respectively, by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, cytoskeleton analysis, alkaline phosphatase activity assay, alizarin red staining, and real-time polymerase chain reaction. Western blots analysis was used to explore the role of PI3K/Akt pathway.</p><p><strong>Results: </strong>The viability, osteogenic differentiation, and mineralization of MC3T3-E1 cells were significantly decreased by high glucose. All observed osteogenic dysfunction were inhibited by CGF-e. Moreover, the PI3K/Akt pathway was activated by CGF-e.</p><p><strong>Conclusions: </strong>It was concluded that the soluble factors released by CGF could significantly attenuate high glucose-mediated MC3T3-E1 cells osteogenic dysfunction through the PI3K/Akt pathway.</p>","PeriodicalId":13309,"journal":{"name":"Implant Dentistry","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/ID.0000000000000921","citationCount":"4","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Implant Dentistry","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1097/ID.0000000000000921","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"Dentistry","Score":null,"Total":0}
引用次数: 4
Abstract
Introduction: The aim of this study is to investigate the effects of Concentrate Growth Factors Extract (CGF-e) on the proliferation and osteogenic differentiation of MC3T3-E1 cells under high glucose condition.
Materials and methods: MC3T3-E1 cells were divided into 4 groups including normal glucose (5.5-mM) group (control), high glucose (25.5-mM) group, normal glucose + CGF-e group, and high glucose + CGF-e group. The proliferation, osteogenic differentiation and mineralization of osteoblasts were evaluated, respectively, by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, cytoskeleton analysis, alkaline phosphatase activity assay, alizarin red staining, and real-time polymerase chain reaction. Western blots analysis was used to explore the role of PI3K/Akt pathway.
Results: The viability, osteogenic differentiation, and mineralization of MC3T3-E1 cells were significantly decreased by high glucose. All observed osteogenic dysfunction were inhibited by CGF-e. Moreover, the PI3K/Akt pathway was activated by CGF-e.
Conclusions: It was concluded that the soluble factors released by CGF could significantly attenuate high glucose-mediated MC3T3-E1 cells osteogenic dysfunction through the PI3K/Akt pathway.
期刊介绍:
Cessation. Implant Dentistry, an interdisciplinary forum for general practitioners, specialists, educators, and researchers, publishes relevant clinical, educational, and research articles that document current concepts of oral implantology in sections on biomaterials, clinical reports, oral and maxillofacial surgery, oral pathology, periodontics, prosthodontics, and research. The journal includes guest editorials, letters to the editor, book reviews, abstracts of current literature, and news of sponsoring societies.