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  • ISSN 1674-8301
  • CN 32-1810/R
Volume 36 Issue 1
Jan.  2022
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Abstract
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Wenqian Xia, Xiao Han, Lin Wang. E26 transformation-specific 1 is implicated in the inhibition of osteogenic differentiation induced by chronic high glucose by directly regulating Runx2 expression[J]. The Journal of Biomedical Research, 2022, 36(1): 39-47. DOI: 10.7555/JBR.35.20210123
Citation: Wenqian Xia, Xiao Han, Lin Wang. E26 transformation-specific 1 is implicated in the inhibition of osteogenic differentiation induced by chronic high glucose by directly regulating Runx2 expression[J]. The Journal of Biomedical Research, 2022, 36(1): 39-47. DOI: 10.7555/JBR.35.20210123
shu

E26 transformation-specific 1 is implicated in the inhibition of osteogenic differentiation induced by chronic high glucose by directly regulating Runx2 expression

  • 1.

    Key Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu 211166, China

  • 2.

    Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, Jiangsu 210009, China

  • 3.

    The Affiliated Nantong Stomatological Hospital of Nantong University, Nantong, Jiangsu 226001, China

More Information
  • Corresponding author:

    Xiao Han, Key Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, 101 Longmian Avenue, Nanjing, Jiangsu 211166, China. Tel: +86-25-86869426, E-mail: hanxiao@njmu.edu.cn

    Lin Wang, Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, 1 Shanghai Road, Nanjing, Jiangsu 210009, China. Tel: +86-25-69593065, E-mail: lw603@njmu.edu.cn

  • Received Date: July 27, 2021
  • Revised Date: October 07, 2021
  • Accepted Date: October 14, 2021
  • Available Online: December 29, 2021
    Graphical Abstract
    • Abstract
  • Chronic high glucose (HG) plays a crucial role in the pathogenesis of diabetes-induced osteoporosis by inhibiting the differentiation and proliferation of osteoblasts. This study aims to examine the role of E26 transformation-specific 1 (ETS1) in the inhibition of osteoblast differentiation and proliferation caused by chronic HG, as well as the underlying mechanism. Chronic HG treatment downregulated ETS1 expression and inhibited differentiation and proliferation of MC3T3-E1 cells. Downregulation of ETS1 expression inhibited the differentiation and proliferation of MC3T3-E1 cells under normal glucose conditions, and ETS1 overexpression attenuated the damage to cells exposed to chronic HG. In addition, ETS1 overexpression reversed the decrease in runt-related transcription factor 2 (Runx2) expression in MC3T3-E1 cells treated with chronic HG. Using chromatin immunoprecipitation (ChIP) and luciferase reporter assays, we confirmed that ETS1 directly bound to and increased the activity of the Runx2 promoter. In summary, our study suggested that ETS1 was involved in the inhibitory effect of chronic HG on osteogenic differentiation and proliferation and may be a potential therapeutic target for diabetes-induced osteoporosis.
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    • References (30)
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