Inhibitory effect of miR‑182‑5p on retinal neovascularization by targeting angiogenin and BDNF

Chenyue Li1, Hongxuan Lie1, Weifeng Sun1

  • 1Department of Ophthalmology, Changhai Hospital, Naval Medical University, Shanghai 200082, P.R. China.

Molecular Medicine Reports
|December 22, 2021
PubMed

Insights

MicroRNA-182-5p targets Angiogenin and BDNF to inhibit retinal neovascularization (RNV). This microRNA-based therapy shows potential for treating RNV diseases by improving retinal cell function under hypoxia.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Genetics

Background:

  • Retinal neovascularization (RNV) is a major cause of vision loss, often linked to hypoxia in conditions like diabetic retinopathy.
  • Anti-VEGF therapy is standard but not universally effective, necessitating new therapeutic targets.
  • The roles of Angiogenin (ANG) and brain-derived neurotrophic factor (BDNF) in RNV require further clarification.

Purpose of the Study:

  • To investigate the microRNA-mediated regulation of ANG and BDNF in hypoxia-induced retinal neovascularization.
  • To explore the therapeutic potential of targeting ANG and BDNF using microRNAs for RNV treatment.

Main Methods:

  • Utilized an oxygen-induced retinopathy mouse model and human retinal microvascular endothelial cells (HRECs) under hypoxic conditions.
  • Assessed the expression levels of miR-182-5p, ANG, and BDNF.
  • Manipulated miR-182-5p levels and evaluated the impact on ANG/BDNF expression and HREC function.

Main Results:

  • Downregulation of miR-182-5p and upregulation of ANG and BDNF were observed in hypoxic conditions.
  • Overexpression of miR-182-5p significantly reduced ANG and BDNF expression in HRECs.
  • miR-182-5p-mediated knockdown of ANG and BDNF improved hypoxia-induced HREC dysfunction, including viability, migration, and tube integrity.

Conclusions:

  • MicroRNA-dependent regulation of ANG and BDNF plays a crucial role in the retinal microvascular response to hypoxia.
  • miR-182-5p demonstrates potential as a therapeutic agent for RNV diseases by modulating ANG and BDNF expression.