June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Suppression of MiR-18b on high-glucose-induced proliferation of human retinal endothelial cells by targeting insulin growth factor-1(IGF-1)/IGF1R signaling pathways
Author Affiliations & Notes
  • Jinhui Wu
    Ophthalmology, Changhai Hospital, Shanghai, China
    Departments of Ophthalmology & Visual Sciences, University of Louisville, Louisville, KY
  • Footnotes
    Commercial Relationships Jinhui Wu, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 40. doi:
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    • Get Citation

      Jinhui Wu; Suppression of MiR-18b on high-glucose-induced proliferation of human retinal endothelial cells by targeting insulin growth factor-1(IGF-1)/IGF1R signaling pathways. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):40.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: MicroRNAs (miRNAs) are important in the proliferation and migration of endothelial cells and have been shown to be involved in diabetic retinopathy (DR). In the present study, the roles of miR-18b in high glucose induced proliferation of human retinal endothelial cells (HRECs) were investigated in vitro

Methods: 1) MiR-18b mimics and inhibitor transfection were used to determine the role of miR-18b in proliferation of HRECs and expression of VEGF; 2) mechanisms by which miR-18b affected the proliferation of HRECs were studied by analysis of up- or down-regulation of insulin growth factor (IGF-1)

Results: High glucose medium induced the proliferation of HRECs and the down-regulated the expression of miR-18b in proliferative HRECs. The decreased miR-18b expression promoted VEGF expression. Mechanistically, IGF-1 was identified as the target of miR-18b. Over expression of IGF-1 could antagonize the role of up-regulated miR-18b. In contrast, silencing IGF-1 induced similar effects of down-regulated miR-18b, which increased VEGF expression.

Conclusions: MiR-18b could suppress proliferation of HRECs and production of VEGF through inhibiting IGF-1/IGF-1R signaling pathway, which may provide a new explanation of the mechanism of miR-18b-mediated inhibition of HRECs proliferation, as well as a potential therapeutic target for proliferative DR.

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