July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018

MicroRNA-184 Downregulation Contributes to Corneal Neovascularization
Author Affiliations & Notes
  • rongrong zong
    Eye Institute of Xiamen University, Xiamen, China
  • Zuguo Liu
    Eye Institute of Xiamen University, Xiamen, China
  • yueping zhou
    Eye Institute of Xiamen University, Xiamen, China
  • Footnotes
    Commercial Relationships   rongrong zong, None; Zuguo Liu, None; yueping zhou, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 3339. doi:https://doi.org/
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      rongrong zong, Zuguo Liu, yueping zhou;
      MicroRNA-184 Downregulation Contributes to Corneal Neovascularization. Invest. Ophthalmol. Vis. Sci. 2018;59(9):3339. doi: https://doi.org/.

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

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Abstract

Purpose :
microRNA-184 (miR-184) is an endogenous short non-coding RNA and abundantly expressed in the corneas. We further evaluated the association between miR-184 expression and corneal neovascularization using both alkali burn and suture models in rat corneas.

Methods :
Expression level of miR-184 in the rat corneas was measured by TaqMan qPCR assay. Realtime RT-PCR or western blot was performed to detect the potential target genes of miR-184. MicroRNA-184 mimic was also topically administered to rat corneas. Human umbilical vein endothelial cells (HUVECs) were transfected with mimic and inhibitor of miR184 using Lipofectamine RNAiMAX reagent. CCK8 assay and scratch wound test were carried out to evaluate the effects of miR-184 on cell proliferation and migration. Tube formation assay was also conducted.

Results : The expression of miR-184 was significantly decreased, whereas Wnt signaling pathway factors were upregulated in both alkali burn and suture models of rat corneas. The corneal neovascularization induced by s was ameliorated by topical administration of miR-184.Transfection of miR-184 into HUVECs significantly suppressed the cell proliferation and migration. Furthermore, miR-184 inhibited the tube formation of HUVECs cells.

Conclusions :
Our results demonstrate that miR-184 negatively regulates corneal neovascularization in two different animal models. miR-184 may be a novel therapeutic strategy to prevent neovasculaturization in the cornea.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.

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