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Updated: Oct 9, 2025

Retinal Explant of the Adult Mouse Retina as an Ex Vivo Model for Studying Retinal Neurovascular Diseases
Published on: December 9, 2022
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.
Abstract:
Retinal neovascularization (RNV) is a type of serious vision‑threating disease, commonly induced by hypoxia of ischemic retinopathy, which happens in various ocular diseases including diabetic retinopathy and retinopathy of prematurity. In clinical work, anti‑VEGF therapy is the preferred strategy for treating RNV. However, not all cases are sensitive to anti‑VEGF injection. It is urgent and necessary to develop novel targets for inhibiting neovascularization in ocular diseases. Angiogenin (ANG) and brain‑derived neurotrophic factor (BDNF) are implicated in angiogenesis, although their regulation and effects in RNV remain to be elucidated. microRNA (miRNA) is a type of small non‑coding RNA, which can modulate targets by degrading transcripts or inhibiting protein translation. In the present study, miRNA‑mediated modulation of ANG and BDNF was explored in an oxygen‑induced retinopathy mouse model and human retinal microvascular endothelial cells (HRECs) under hypoxia. The results showed that downregulation of miR‑182‑5p and upregulation of ANG and BDNF were found in vivo and in vitro. Overexpression of miR‑182‑5p suppressed the expression of ANG and BDNF significantly in HRECs under hypoxia. In addition, knockdown of ANG and BDNF by miR‑182‑5p transfection significantly improved hypoxia‑induced HRECs dysfunctions, including enhancing cell viability, reducing cell migration and improved tube integrity. In conclusion, miRNA‑dependent regulation on ANG and BDNF indicates a critical role in hypoxia‑induced retinal microvascular response. miR‑182‑5p‑based therapy can influence the expression of ANG and BDNF, which demonstrates the potential for treating RNV diseases.
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.

