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Updated: Jun 20, 2026

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Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis
Published on: June 3, 2018
Selective Laser Trabeculoplasty Mitigates Dexamethasone-Induced Myofibroblast-Like Transformation and Dysfunction in
Cheng Lai1, Lian Liu1, Min Zhu1
1Department of Ophthalmology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Current Eye Research
|June 19, 2026
Summary
Selective laser trabeculoplasty (SLT) reverses early signs of glucocorticoid-induced glaucoma (GIG) in human trabecular meshwork cells. SLT normalizes fibrotic changes and restores cellular functions, suggesting a disease-modifying potential for GIG.
Area of Science:
- Ophthalmology
- Cell Biology
- Biochemistry
Background:
- Glucocorticoid-induced glaucoma (GIG) is characterized by trabecular meshwork (TM) fibrosis, leading to impaired aqueous humor outflow.
- Selective laser trabeculoplasty (SLT) effectively lowers intraocular pressure, but its cellular mechanisms in GIG are not fully understood.
Purpose of the Study:
- To investigate if SLT can reverse the fibrotic phenotype in a steroid-treated primary human TM cell model.
- To assess SLT's ability to restore TM cell function following glucocorticoid exposure.
Main Methods:
- Primary human TM cells were treated with dexamethasone (DEX) to induce fibrosis.
- Cells were subsequently treated with or without SLT.
- Analysis included Western blot, immunofluorescence, scratch and transwell migration assays, phagocytosis, and proliferation assays.
Main Results:
- Dexamethasone induced myofibroblast-like morphology, extracellular matrix accumulation, and elevated myofibroblast markers.
- SLT significantly reduced these fibrotic changes, approaching control levels.
- SLT abolished DEX-enhanced migration and partially restored DEX-impaired phagocytosis and proliferation.
Conclusions:
- SLT mitigates early glucocorticoid-induced TM fibrosis.
- SLT restores key cellular functions in TM cells affected by steroids.
- These findings support SLT as a potential disease-modifying therapy for GIG.
