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Updated: Feb 14, 2026
Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye
Published on: June 20, 2015
Micro RNA-1298 opposes the effects of chronic oxidative stress on human trabecular meshwork cells via targeting on
Wu Ruibin1, Xiaowei Zheng1, Jiaying Chen1
1Department of Ophthalmolog, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, 515000, China.
Objective:
This study aimed to investigate the effect and potential mechanism of miR-1298 in the progression of human trabecular meshwork (HTM) cells.
Material And Methods:
Expression of miR-1298 was assessed by quantitative real time PCR (qRT-PCR), as well as in HTM-1 and HTM-2 cells. Mature miR-1298 mimic, miR-1298 inhibitor, and si-EIF4E3 and their corresponding controls were transfected into HTM-1 and HTM-2 to obtain stable HTM cells. Luciferase reporter assay was used to verify regulation between miR-1298 and EIF4E3. Cytotoxicity and Oxidative damage were assessed using commercial kits, and apoptosis was determined using flow cytometry. ECM and apoptosis related factors were determined using qRT-PCR and western blotting, as well as the pathway related factors.
Results:
The expression of miR-1298 was significantly decreased both in glaucoma and HTM cells. MiR-1298 mimic could significantly inhibit the increase of cytotoxicity, apoptosis, accumulation of carbonylated proteins and ECM induced by COS, but miR-1298 inhibitor could obviously promote the increase effects caused by COS in HTM cells. EIF4E3 was a downstream target of miR-1298. Sliced EIF4E3 could significantly inhibit the increase effects induced miR-1298 inhibitor in HTM cells under COS. The expression levels of TGF-β2 and Smad4 were significantly increased, and Wnt3a and β-cantenin were obviously decreased under COS, and miR-1298 inhibitor could markedly promote this increase effect, while sliced EIF4E3 could reverse the effect of miR-1298 under COS.
Conclusions:
miR-1298 could protect HTM cells to against damage caused by COS via inhibiting TGF-β2/Smad4 pathway and activating canonical Wnt pathway.
Insights
MicroRNA-1298 (miR-1298) protects human trabecular meshwork cells from damage. It achieves this by inhibiting the TGF-β2/Smad4 pathway and activating the Wnt pathway, offering a potential therapeutic target for glaucoma.
Area of Science:
- Ophthalmology and Molecular Biology
- Cell Biology and Genetics
Background:
- Glaucoma is a leading cause of irreversible blindness.
- Human trabecular meshwork (HTM) cells play a crucial role in regulating intraocular pressure.
- Dysregulation of microRNAs is implicated in the pathogenesis of glaucoma.
Purpose of the Study:
- To investigate the role and mechanism of miR-1298 in HTM cells.
- To determine if miR-1298 affects cellular responses to oxidative stress.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) for gene expression analysis.
- Transfection of miR-1298 mimics/inhibitors and si-EIF4E3 in HTM cells.
- Luciferase reporter assays to confirm target interaction.
- Assessment of cytotoxicity, oxidative damage, apoptosis, and extracellular matrix (ECM) production.
Main Results:
- miR-1298 expression was reduced in glaucoma and HTM cells.
- miR-1298 mimic reduced cytotoxicity, apoptosis, and ECM accumulation induced by COS.
- EIF4E3 was identified as a direct target of miR-1298.
- miR-1298 regulated TGF-β2/Smad4 and Wnt signaling pathways.
Conclusions:
- miR-1298 protects HTM cells against COS-induced damage.
- The protective effect involves inhibition of the TGF-β2/Smad4 pathway.
- Activation of the canonical Wnt pathway contributes to miR-1298's protective function.
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