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Article

miR‑192 is upregulated in T1DM, regulates pancreatic β‑cell development and inhibits insulin secretion through suppressing GLP‑1 expression

  • Authors:
    • Wen Pan
    • Yanan Zhang
    • Chun Zeng
    • Fen Xu
    • Jinhua Yan
    • Jianping Weng
  • View Affiliations / Copyright

    Affiliations: Department of Endocrinology and Metabolism, The Third Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510630, P.R. China, Department of Emergency, The Third Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510630, P.R. China
  • Pages: 2717-2724
    |
    Published online on: July 17, 2018
       https://doi.org/10.3892/etm.2018.6453
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Abstract

MicroRNAs (miRs) post‑translationally regulate gene expression by specifically binding to the mRNA of their target genes. The aim of the present study was to determine the effect of miR‑192 on pancreatic β‑cell development. The serum levels of miR‑192 in type 1 diabetes mellitus (T1DM) and streptozotocin‑induced rats were determined, and were revealed to be elevated compared with those in healthy patients and normal rats, respectively. Western blot and reverse transcription‑quantitative polymerase chain reaction analysis indicated that miR‑192 suppressed the expression of glucagon‑like peptide‑1 (GLP‑1), a potent insulin secretagogue. Ectopic expression of miR‑192 inhibited cell proliferation and promoted apoptosis of NIT‑1 cells, while miR‑192 inhibitor had the opposite effect. Collectively, the present results revealed that miR‑192 was elevated in T1DM, and is implicated in pancreatic β‑cell development through regulation of cell proliferation and apoptosis, thereby suppressing insulin secretion. Furthermore, miR‑192 suppressed GLP‑1 expression, thereby further promoting T1DM. The present study suggested that miR‑192 is a novel molecular target for the management or prevention of T1DM.
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Copy and paste a formatted citation
Spandidos Publications style
Pan W, Zhang Y, Zeng C, Xu F, Yan J and Weng J: miR‑192 is upregulated in T1DM, regulates pancreatic β‑cell development and inhibits insulin secretion through suppressing GLP‑1 expression. Exp Ther Med 16: 2717-2724, 2018.
APA
Pan, W., Zhang, Y., Zeng, C., Xu, F., Yan, J., & Weng, J. (2018). miR‑192 is upregulated in T1DM, regulates pancreatic β‑cell development and inhibits insulin secretion through suppressing GLP‑1 expression. Experimental and Therapeutic Medicine, 16, 2717-2724. https://doi.org/10.3892/etm.2018.6453
MLA
Pan, W., Zhang, Y., Zeng, C., Xu, F., Yan, J., Weng, J."miR‑192 is upregulated in T1DM, regulates pancreatic β‑cell development and inhibits insulin secretion through suppressing GLP‑1 expression". Experimental and Therapeutic Medicine 16.3 (2018): 2717-2724.
Chicago
Pan, W., Zhang, Y., Zeng, C., Xu, F., Yan, J., Weng, J."miR‑192 is upregulated in T1DM, regulates pancreatic β‑cell development and inhibits insulin secretion through suppressing GLP‑1 expression". Experimental and Therapeutic Medicine 16, no. 3 (2018): 2717-2724. https://doi.org/10.3892/etm.2018.6453
Copy and paste a formatted citation
x
Spandidos Publications style
Pan W, Zhang Y, Zeng C, Xu F, Yan J and Weng J: miR‑192 is upregulated in T1DM, regulates pancreatic β‑cell development and inhibits insulin secretion through suppressing GLP‑1 expression. Exp Ther Med 16: 2717-2724, 2018.
APA
Pan, W., Zhang, Y., Zeng, C., Xu, F., Yan, J., & Weng, J. (2018). miR‑192 is upregulated in T1DM, regulates pancreatic β‑cell development and inhibits insulin secretion through suppressing GLP‑1 expression. Experimental and Therapeutic Medicine, 16, 2717-2724. https://doi.org/10.3892/etm.2018.6453
MLA
Pan, W., Zhang, Y., Zeng, C., Xu, F., Yan, J., Weng, J."miR‑192 is upregulated in T1DM, regulates pancreatic β‑cell development and inhibits insulin secretion through suppressing GLP‑1 expression". Experimental and Therapeutic Medicine 16.3 (2018): 2717-2724.
Chicago
Pan, W., Zhang, Y., Zeng, C., Xu, F., Yan, J., Weng, J."miR‑192 is upregulated in T1DM, regulates pancreatic β‑cell development and inhibits insulin secretion through suppressing GLP‑1 expression". Experimental and Therapeutic Medicine 16, no. 3 (2018): 2717-2724. https://doi.org/10.3892/etm.2018.6453
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