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Downregulation of miR-127-5p promotes idiopathic epiretinal membrane development via GLUL-mediated Müller cell
Jianing Ying1, Qian Gui1, Shanshan Hua2
1Ningbo Eye Hospital, Wenzhou Medical University, Ningbo, Zhejiang, China.
Abstract:
Idiopathic epiretinal membrane (iERM) represents a fibrocellular proliferation on retinal surface associated with vision loss, with underlying molecular mechanisms that remain undefined. The current work aimed to assess miR-127-5p for its role in the regulation of retinal Müller cell activity in iERM. We analyzed miRNA expression profiles in vitreous samples from iERM patients and controls. The regulatory relationship between miR-127-5p and GLUL (glutamine synthetase) was verified through dual-luciferase reporter assays and molecular studies. The functional effects of the miR-127-5p/GLUL axis manipulation were evaluated in rat retinal Müller cells using proliferation, migration, invasion, and apoptosis assays. miR-127-5p showed significant downregulation in iERM cases. miR-127-5p overexpression in retinal Müller cells suppressed their proliferative, invasive, and migratory capabilities, while inducing apoptotic cell death. GLUL was shown to be directly targeted by miR-127-5p and was upregulated in iERM patients. Knockdown of GLUL phenocopied the impacts of miR-127-5p overexpression, with its overexpression reversing miR-127-5p-associated suppressive effects on Müller cell behavior. These findings suggest miR-127-5p is a key modulator of iERM pathogenesis, functioning through its interaction with GLUL to control retinal Müller cell proliferation and migration. The miR-127-5p/GLUL axis might represent a novel target for iERM treatment.
Insights
MicroRNA-127-5p (miR-127-5p) is downregulated in idiopathic epiretinal membrane (iERM), a condition causing vision loss. Its regulation of Müller cell activity via GLUL offers a potential new therapeutic target for iERM.
Area of Science:
- Ophthalmology
- Molecular Biology
- Cell Biology
Background:
- Idiopathic epiretinal membrane (iERM) is a retinal condition causing vision loss due to fibrocellular proliferation.
- The molecular mechanisms driving iERM pathogenesis are not fully understood.
Purpose of the Study:
- To investigate the role of miR-127-5p in regulating retinal Müller cell activity in iERM.
- To identify the molecular targets and pathways involved in miR-127-5p's function in iERM.
Main Methods:
- Analysis of miRNA expression profiles in vitreous samples from iERM patients and controls.
- Dual-luciferase reporter assays to confirm the regulatory relationship between miR-127-5p and GLUL.
- In vitro functional assays (proliferation, migration, invasion, apoptosis) in rat retinal Müller cells following manipulation of miR-127-5p and GLUL.
Main Results:
- miR-127-5p was significantly downregulated in iERM patients.
- Overexpression of miR-127-5p suppressed Müller cell proliferation, migration, and invasion, while increasing apoptosis.
- GLUL was identified as a direct target of miR-127-5p and was upregulated in iERM. GLUL knockdown mimicked miR-127-5p effects, and GLUL overexpression reversed them.
Conclusions:
- miR-127-5p plays a critical role in iERM pathogenesis by controlling retinal Müller cell behavior.
- The miR-127-5p/GLUL axis is a key regulatory pathway in iERM.
- This axis represents a potential novel therapeutic target for treating iERM.
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