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MiR-423-5p promotes Müller cell activation via targeting NGF signaling in diabetic retinopathy
Yanqiu Liu1, Zifan Xu1, Haohan Zheng1
1Department of Ophthalmology, The Affiliated Wuxi People's Hospital of Nanjing Medical University, 299 Qingyang Road, Wuxi, Jiangsu 214023, People's Republic of China.
Aims:
Diabetic retinopathy (DR) is a common microvascular complication of diabetes mellitus and one of the major causes of visual impairment and blindness in industrialized countries. The early neuro-glial perturbations, especially retinal Müller cells (rMC) activation, intimately associated with the vascular alterations. MicroRNAs (miRNAs) have been reported to play critical roles in the progression of DR. Here, we aimed to further explore the role and underlying mechanism of miR-423-5p in Müller cell activation in streptozotocin (STZ)-induced diabetic mice and oxygen-induced retinopathy (OIR) model.
Materials And Methods:
Retinal histology, optical coherence tomography (OCT) and biochemical markers were assessed.
Key Findings:
Our data revealed that the expression of miR-423-5p was significantly increased under high-glucose environment. We also demonstrated that miR-423-5p overexpression markedly accelerated retinal vascular leakage, leukocytosis, and rMC activation. This response was ameliorated in animals pre-treated with the inhibition of miR-423-5p. Specifically, miR-423-5p bound to the nerve growth factor (NGF) 3' UTR region to induce its silencing. NGF inhibition significantly promoted retinal microvascular dysfunction.
Significance:
These findings demonstrate that miR-423-5p is a critical miRNA that promotes microvascular dysfunction in DR.
Insights
MicroRNA-423-5p promotes diabetic retinopathy (DR) by activating retinal Müller cells and causing microvascular dysfunction. Inhibiting miR-423-5p ameliorates these DR-related changes, highlighting its role in the disease.
Area of Science:
- Ophthalmology
- Molecular Biology
- Endocrinology
Background:
- Diabetic retinopathy (DR) is a leading cause of vision loss, characterized by neuro-glial and vascular changes.
- Müller cell (rMC) activation is an early event in DR pathogenesis.
- MicroRNAs (miRNAs) are implicated in DR progression.
Purpose of the Study:
- To investigate the role of miR-423-5p in Müller cell activation.
- To elucidate the mechanism of miR-423-5p in diabetic retinopathy (DR).
Main Methods:
- Utilized streptozotocin (STZ)-induced diabetic mice and oxygen-induced retinopathy (OIR) models.
- Assessed retinal histology, optical coherence tomography (OCT), and biochemical markers.
- Investigated miRNA-mRNA interactions using 3' UTR luciferase assays.
Main Results:
- miR-423-5p expression increased in high-glucose conditions.
- Overexpression of miR-423-5p accelerated vascular leakage, leukocytosis, and rMC activation.
- miR-423-5p directly silences nerve growth factor (NGF), promoting microvascular dysfunction.
Conclusions:
- miR-423-5p is a key driver of microvascular dysfunction in diabetic retinopathy (DR).
- Targeting miR-423-5p may offer a therapeutic strategy for DR.
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