Functional morphology of the trabecular meshwork in primate eyes

Lütjen–Drecoll, Elke

doi:10.1016/s1350-9462(98)00011-1

Cited by 218 publications

(178 citation statements)

References 67 publications

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“…In addition, baseline SC-CSA dropped from 4,597 ± 2,503 µm 2 to 3,588 ± 1,198 µm 2 (mean ± standard deviation) with smooth muscle activity suppression. Together, with the insertion of anterior tendons from the ciliary muscle which insert into the outer lamellated and cribiform TM 17 , this implies a control system to maintain SC patency involving smooth muscle. Further study is merited.…”

Section: Representative Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…The posterior TM is anchored into the ciliary muscle via anterior tendons of the longitudinal muscle cells which insert into the outer lamellated and cribiform TM 17 . Ciliary muscle (CM) activity may increase TM tautness, mimicking elevated TM stiffness 17 . The ability to observe alterations in resistance to SC collapse induced by perturbations of smooth muscle has been shown in an animal model 18 .…”

Section: Introductionmentioning

confidence: 99%

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Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye

Kagemann

Wang

Wollstein

et al. 2015

JoVE

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The mechanical characteristics of the trabecular meshwork (TM) are linked to outflow resistance and intraocular pressure (IOP) regulation. The rationale behind this technique is the direct observation of the mechanical response of the TM to acute IOP elevation. Prior to scanning, IOP is measured at baseline and during IOP elevation. The limbus is scanned by spectral-domain optical coherence tomography at baseline and during IOP elevation (ophthalmodynamometer (ODM) applied at 30 g force). Scans are processed to enhance visualization of the aqueous humor outflow pathway using ImageJ. Vascular landmarks are used to identify corresponding locations in baseline and IOP elevation scan volumes. Schlemm canal (SC) cross-sectional area (SC-CSA) and SC length from anterior to posterior along its long axis are measured manually at 10 locations within a 1 mm segment of SC. Mean inner to outer wall distance (short axis length) is calculated as the area of SC divided by its long axis length. To examine the contribution of adjacent tissues to the effect IOP elevations, measurements are repeated without and with smooth muscle relaxation with instillation of tropicamide. TM migration into SC is resisted by TM stiffness, but is enhanced by the support of its attachment to adjacent smooth muscle within the ciliary body. This technique is the first to measure the living human TM response to pressure elevation in situ under physiological conditions within the human eye. Video LinkThe video component of this article can be found at

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Section: Representative Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye

Kagemann

Wang

Wollstein

et al. 2015

JoVE

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“…Aqueous humor is produced by the ciliary epithelium, delivered to the anterior chamber, and then drains through the trabecular meshwork (TM) into Schlemm's canal and the episcleral veins (Morrison & Acott, 2003). The major resistance to aqueous outflow occurs at the TM, which is comprised of a complex extracellular matrix (ECM) of collagen beams lined with endothelial-like cells (Lutjen-Drecoll, 1999.…”

Section: Introductionmentioning

confidence: 99%

Cochlin and glaucoma: A mini-review

2005

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Primary open angle glaucoma (POAG) is a leading cause of late onset, progressive, irreversible blindness and, although its etiology is poorly understood, elevated intraocular pressure (IOP) often appears to be a contributory factor. Proteomic and Western analyses of trabecular meshwork (TM) from patients with POAG and age-matched controls originally implicated cochlin as possibly contributing to glaucoma pathogenesis. Cochlin deposits were subsequently detected in glaucomatous but not in control TM and older glaucomatous TM was found to contain higher levels of cochlin and significantly lower amounts of collagen type II. More recently, similar results were reported in DBA/2J mice, which at older ages develop elevated IOP, retinal ganglion cell degeneration, and optic nerve damage. Notably, cochlin was absent in TM from C57BL/6J, CD1, and BALBc/ByJ mice, which do not exhibit elevated IOP or glaucoma. Cochlin was found in the TM of very young DBA/2J mice, prior to elevated IOP, suggesting that over time the protein may contribute to the events leading to increased IOP and optic nerve damage. Here we review these findings and describe how future studies in DBA/2J mice can help resolve whether cochlin plays a causal role in mechanisms of POAG and elevated IOP.

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“…These spaces gradually become smaller as they get closer to SC, and the density of the TM cells and ECM is relatively high in this area, resulting in a higher resistance to flow. The tissues of the conventional outflow pathway have unique morphological and functional properties with subtle complexities (23) . The functional properties of the TM are often affected in individuals of increasing age and those with ocular disease, such as POAG (24) .…”

Section: Physiology Of Aqueous Humor Outflowmentioning

confidence: 99%