Trabecular Meshwork
Trabecular Meshwork - Related Videos
09:03
Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye
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Cited by 7 •
2015
Trabecular meshwork (TM) migration into Schlemm’s canal space can be induced by acute pressure elevation by ophthalmodynamometer, and observed by spectral domain optical coherence tomography. The goal of this method is to quantify the morphometric response of the living outflow tract to acute pressure elevation in living tissues in situ.
13:47
Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis
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Cited by 5 •
2018
Here, we describe a protocol for a reproducible laser capture microdissection (LCM) for isolating trabecular meshwork (TM) for downstream RNA analysis. The ability to analyze changes in gene expression in the TM will help in understanding the underlying molecular mechanisms of TM-related ocular diseases.
09:36
Outer-Boundary Assisted Segmentation and Quantification of Trabecular Bones by an Imagej Plugin
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2018
We present a workflow for segmenting and quantifying trabecular bones for 2D and 3D images based on the bone's outer boundary using an ImageJ plugin. This approach is more efficient and accurate than the current manual hand-contouring approach, and provides layer-by-layer quantifications, which are not available in current commercial software.
06:59
Trabecular Bone Microarchitecture Evaluation in an Osteoporosis Mouse Model
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Cited by 3 •
2023
This protocol presents an economical and efficient method for quantitative evaluation of bone microarchitecture in a mouse model of osteoporosis by combining Hematoxylin-Eosin (HE) staining and micro-computed tomography (Micro-CT) techniques.
03:24
Anterior Eye Segment Dissection: A Method to Isolate Cornea Bearing Anterior Segment from Porcine Eye
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2025
In this video, we demonstrate the dissection of the cornea-bearing anterior segment of the porcine eye. The isolated segment can be used for organ culturing to study the pathophysiology of eye disorders.
FAQs
Outflow depends on passage through porous beams and the endothelial lining before aqueous humor reaches Schlemm’s canal. These structures do not simply provide an open route; their organization contributes to resistance, while cellular contractility and extracellular matrix can further alter how readily fluid moves. Consequently, structural and biomechanical changes can affect intraocular pressure.
Cholinergic drugs enhance aqueous humor drainage indirectly by causing the ciliary muscle to contract. That contraction changes the mechanical conditions governing outflow through the trabecular meshwork, helping fluid move toward Schlemm’s canal. In pharmacology, this mechanism links receptor-directed drug action to reduced resistance and, ultimately, lower intraocular pressure.
Rho kinase inhibitors act by relaxing trabecular cells, which reduces resistance to aqueous humor outflow. This mechanism differs from the contractile action associated with cholinergic drugs: instead of promoting drainage through ciliary muscle contraction, it directly changes the cellular state of the drainage tissue. The resulting increase in outflow can support intraocular-pressure reduction.
Extracellular matrix resistance is one of the variables that controls aqueous humor outflow, alongside cellular contractility. If this resistance changes, the ease with which fluid crosses the drainage pathway also changes. Considering both factors helps pharmacologists interpret how a treatment may alter outflow and intraocular pressure rather than focusing on cellular contraction alone.
The key outcomes are changes in aqueous humor drainage, outflow resistance, and intraocular pressure. These measures connect a drug’s local action with its therapeutic objective. A treatment that enhances drainage or lowers resistance may reduce intraocular pressure, while the broader clinical purpose is to help protect vision in glaucoma.
It provides a setting for comparing distinct ways to improve aqueous humor outflow. Investigators can examine whether a candidate acts through ciliary muscle contraction, trabecular-cell relaxation, or altered resistance in the drainage pathway. Linking that mechanism to intraocular-pressure reduction helps evaluate pharmacological strategies intended to protect vision.