Investigative Ophthalmology & Visual Science Cover Image for Volume 65, Issue 7
June 2024
Volume 65, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2024
MiR 15a 5p inhibits angiogenesis and suppresses inflammation and fibrosis via targeting VEGF and smad2 in ocular neovascularization
Author Affiliations & Notes
  • Xiaorong Li
    Tianjin Medical University Eye Hospital, Tianjin, Tianjin, China
  • Xiaomin Zhang
    Tianjin Medical University Eye Hospital, Tianjin, Tianjin, China
  • Hui Zhang
    Tianjin Medical University Eye Hospital, Tianjin, Tianjin, China
  • Xinyue Yu
    Tianjin Medical University Eye Hospital, Tianjin, Tianjin, China
  • Footnotes
    Commercial Relationships   Xiaorong Li None; Xiaomin Zhang None; Hui Zhang None; Xinyue Yu None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science June 2024, Vol.65, OD62. doi:
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      Xiaorong Li, Xiaomin Zhang, Hui Zhang, Xinyue Yu; MiR 15a 5p inhibits angiogenesis and suppresses inflammation and fibrosis via targeting VEGF and smad2 in ocular neovascularization. Invest. Ophthalmol. Vis. Sci. 2024;65(7):OD62.

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

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Abstract

Purpose : We aim to determine the therapeutic role of miR-15a-5p on fundus neovascularization and reveal its advantages in comparison to anti-VEGF therapy.

Methods : PCR measured miR-15a-5p levels in plasma, plasma sEVs, and vitreous of NDM, DM, NPDR and PDR patients. OIR and CNV models were used to study the effect of intravitreal miR-15a-5p on neovascularization. Retinal structure and function were analyzed using OCT and ERG, comparing the results with anti-VEGF treatment. Inflammatory and pro-fibrotic changes were assessed with WB, PCR, and immunofluorescence. Systemic safety assessments were performed, covering body weight, blood markers, and liver/kidney structure. MiR-15a-5p knockout mice were used to verify the inhibitory effect on neovascularization. In vitro experiments involved HRMECs, RPE cells, and rMC-1 cells, with TGF-β inducing endothelial-mesenchymal transition and inflammatory activation in rMC-1 cells. PCR, WB, and dual-luciferase assays confirmed miR-15a-5p's direct regulation of smad2 and VEGF.

Results : MiR-15a-5p was elevated in NPDR and PDR patients' plasma sEVs and vitreous, but not in plasma. In OIR and CNV models, miR-15a-5p inhibited neovascularization similarly to anti-VEGF treatment, but improved retinal non-perfusion area recovery better. Compared to anti-VEGF, miR-15a-5p reduced Müller cell activation, decreased retinal inflammation, promoted vascular attachment to astrocytes, and facilitated reconstruction. MiR-15a-5p knockout mice showed enhanced neovascularization, which could be reversed by miR-15a-5p injection. Additionally, miR-15a-5p improved retinal structure/function and was safer than anti-VEGF in growing mice. MiR-15a-5p inhibited TGFβ-induced endothelial cell proliferation/transition and suppressed Müller cell activation and VEGF secretion. Dual-luciferase assays confirmed miR-15a-5p directly down-regulated VEGF and smad2.

Conclusions : MiR-15a-5p decreases retinal neovascularization, supports normal vascular growth, reduces inflammation/fibrosis, and is safer than anti-VEGF for mouse body development and lipid metabolism. MiR-15a-5p may be a potential treatment for pathological neovascularization.

This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.

 

An miR-15a-5p deficiency increases abnormal ocular angiogenesis.

An miR-15a-5p deficiency increases abnormal ocular angiogenesis.

 

Evaluating the safety of intravitreal injection of miR-15a-5p and anti-VEGF in developing OIR mice.

Evaluating the safety of intravitreal injection of miR-15a-5p and anti-VEGF in developing OIR mice.

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