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Updated: Jan 22, 2026

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye
Published on: June 20, 2015
Regulatory effect of miR-144-3p on the function of human trabecular meshwork cells and fibronectin-1
1Postgraduate School, Xuzhou Medical University, Xuzhou Eye Hospital, Xuzhou, Jiangsu 221000, P.R. China.
Abstract:
Role of microRNA (miR)-144-3p in regulating the function of human trabecular meshwork cells (HTMCs) and fibronectin-1 (FN-1) was investigated. HTM cell lines were divided into five groups, of which four groups established oxidative stress HTMC models and one served as a control group. The four model groups were transfected with miR-144-3p independent sequence, inhibitory sequence, over-expression sequence, and the blank group received no transfection. In addition, 40 primary open angle glaucoma patients treated in Xuzhou No. 1 People's Hospital were included in the observation group, and 40 healthy individuals were enrolled as a normal group. RT-qPCR was used for the detection of miR-144-3p expression in serum and cells of patients and healthy people in each group, western blot analysis for FN-1 expression in cells, CCK-8 kit for cell proliferation, and Transwell for cell invasion. The expression of serum miR-144-3p in the observation group was significantly lower than that in the normal group (P<0.05). The cell optical density value in the over-expression group was significantly higher than that in the other groups (P<0.05), and in the inhibition group was significantly lower than that in the other groups (P<0.05). The number of cell-penetration in the over-expression group was significantly higher than that in the other groups (P<0.05). The expression of FN-1 protein in the over-expression group was significantly lower than that in the other four groups (P<0.05), and the expression in the inhibition group was significantly higher than that in the other four groups (P<0.05). The over-expression of miR-144-3p promotes proliferation and invasion of HTMCs by inhibiting the expression of FN-1 in inoxidative stress HTMCs, and is a potential target for glaucoma treatment.
Insights
MicroRNA (miR)-144-3p is downregulated in glaucoma patients. Overexpressing miR-144-3p enhances human trabecular meshwork cell proliferation and invasion by inhibiting fibronectin-1, suggesting its potential as a glaucoma treatment target.
Area of Science:
- Ophthalmology
- Molecular Biology
- Cell Biology
Background:
- Glaucoma is a leading cause of irreversible blindness worldwide.
- Human trabecular meshwork cells (HTMCs) play a crucial role in regulating intraocular pressure.
- Dysregulation of microRNAs has been implicated in the pathogenesis of glaucoma.
Purpose of the Study:
- To investigate the role of microRNA (miR)-144-3p in regulating HTMC function.
- To explore the relationship between miR-144-3p and fibronectin-1 (FN-1) in HTMCs.
- To evaluate the therapeutic potential of miR-144-3p in glaucoma.
Main Methods:
- Establishment of oxidative stress HTMC models.
- Transfection of HTMCs with miR-144-3p sequences (independent, inhibitory, over-expression).
- Quantitative real-time PCR (RT-qPCR) for miR-144-3p expression.
- Western blot analysis for FN-1 protein expression.
- Cell Counting Kit-8 (CCK-8) assay for cell proliferation.
- Transwell assay for cell invasion.
- Analysis of serum miR-144-3p in primary open-angle glaucoma patients and healthy controls.
Main Results:
- Serum miR-144-3p expression was significantly lower in glaucoma patients compared to healthy individuals.
- Overexpression of miR-144-3p significantly increased HTMC proliferation and invasion.
- Overexpression of miR-144-3p significantly decreased FN-1 protein expression in HTMCs.
- Inhibition of miR-144-3p decreased HTMC proliferation and invasion while increasing FN-1 expression.
Conclusions:
- Overexpression of miR-144-3p promotes HTMC proliferation and invasion by inhibiting FN-1 expression.
- miR-144-3p plays a protective role in HTMCs under oxidative stress.
- miR-144-3p represents a potential therapeutic target for glaucoma treatment.
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