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Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis
Published on: June 3, 2018
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Lysyl oxidases in the trabecular meshwork.
Robert J Wordinger1, Abbot F Clark
1*North Texas Eye Research Institute †Department of Cell Biology and Immunology, University of North Texas Health Science Center at Fort Worth, Fort Worth, TX.
Journal of Glaucoma
|October 3, 2014
Summary
Increased extracellular matrix (ECM) stiffness in the trabecular meshwork, driven by specific enzymes and transforming growth factor beta (TGF-β), may cause elevated intraocular pressure in glaucoma.
Area of Science:
- Biochemistry
- Cell Biology
- Ophthalmology
Background:
- The extracellular matrix (ECM) is crucial for tissue homeostasis and cellular function.
- Altered ECM biomechanical properties, such as increased stiffness, are implicated in disease pathogenesis.
- Trabecular meshwork (TM) ECM stiffness is a potential factor in glaucoma development.
Purpose of the Study:
- To investigate the role of ECM cross-linking enzymes and transforming growth factor beta (TGF-β) in TM stiffness.
- To explore the potential link between TM stiffness, aqueous humor outflow resistance, and intraocular pressure (IOP).
Main Methods:
- Analysis of ECM cross-linking enzyme expression (tissue transglutaminase, lysyl oxidase, lysyl oxidase-like 1) in the trabecular meshwork.
- Assessment of the regulation of these enzymes by TGF-β isoforms.
- Correlation of TM stiffness with aqueous humor outflow and IOP in glaucoma models or patient data.
Main Results:
- Specific ECM cross-linking enzymes are expressed in the trabecular meshwork.
- These enzymes are regulated by TGF-β isoforms.
- Elevated TGF-β in glaucoma patients suggests a mechanism for increased TM stiffness.
Conclusions:
- Trabecular meshwork stiffness, mediated by ECM cross-linking enzymes regulated by TGF-β, is a potential contributor to elevated intraocular pressure in glaucoma.
- This mechanism may lead to increased aqueous humor outflow resistance.
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