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Src mediates TGF-β-induced intraocular pressure elevation in glaucoma.
Teruhisa Tsukamoto1,2, Kentaro Kajiwara1, Shigeyuki Nada1
1Department of Oncogene Research, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Journal of Cellular Physiology
|August 26, 2018
Summary
Src kinase plays a key role in transforming growth factor-β (TGF-β)-induced elevation of intraocular pressure (IOP), a major glaucoma risk factor. Inhibiting Src signaling may offer a new therapeutic strategy for glaucoma treatment.
Area of Science:
- Ophthalmology
- Molecular Biology
- Cell Biology
Background:
- Glaucoma is a leading cause of irreversible vision loss worldwide.
- Elevated intraocular pressure (IOP) is a primary risk factor for glaucoma.
- The molecular mechanisms linking transforming growth factor-β (TGF-β) to IOP elevation are not fully understood.
Purpose of the Study:
- To investigate the role of Src kinase in TGF-β-induced intraocular pressure (IOP) elevation.
- To explore Src signaling as a potential therapeutic target for glaucoma.
Main Methods:
- Utilized dasatinib, a Src inhibitor, in rat models to assess IOP.
- Performed mechanistic studies in human trabecular meshwork cells.
- Analyzed TGF-β2-induced changes in cytoskeletal remodeling, cell adhesion, and extracellular matrix (ECM) accumulation.
Main Results:
- Dasatinib suppressed TGF-β2-induced IOP elevation in rats.
- TGF-β2 activated Src signaling in trabecular meshwork cells, leading to increased cytoskeletal remodeling, cell adhesion, and ECM accumulation.
- Src activation suppressed tissue plasminogen activator expression, reducing ECM degradation.
- Src inhibition ameliorated TGF-β2-induced alterations in cell contractility, adhesion, and ECM deposition.
Conclusions:
- Src kinase is critically involved in TGF-β-induced IOP elevation.
- Src signaling pathways mediate key cellular changes contributing to increased IOP.
- Targeting Src signaling presents a promising therapeutic avenue for managing glaucoma.
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