Electron microscopic studies on the trabecular meshwork in glaucoma simplex

Rohen, Johannes W.; Witmer, R

doi:10.1007/bf00496153

Cited by 118 publications

(50 citation statements)

References 7 publications

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“…57 These structures located in the JCT and walls of Schlemm's canal are composed of fibrillar material embedded in homogenous matrix, with banded appearance in some cases, which appear to originate from the sheaths of the elastic-like fibers, as extensively characterized in electron microscopic studies by Rohen, Lutjen-Drecoll, and colleagues who referred to them as sheath-derived plaques.…”

Section: Sheath-derived Plaquesmentioning

confidence: 98%

The Microfibril Hypothesis of Glaucoma: Implications for Treatment of Elevated Intraocular Pressure

Kuchtey

2014

Journal of Ocular Pharmacology and Therapeutics

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Microfibrils are macromolecular aggregates located in the extracellular matrix of both elastic and nonelastic tissues that have essential functions in formation of elastic fibers and control of signaling through the transforming growth factor beta (TGFb) family of cytokines. Elevation of systemic TGFb and chronic activation of TGFb signal transduction are associated with diseases caused by mutations in microfibril-associated genes, including FBN1. A role for microfibrils in glaucoma is suggested by identification of risk alleles in LOXL1 for exfoliation glaucoma and mutations in LTBP2 for primary congenital glaucoma, both of which are microfibrilassociated genes.

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Section: Sheath-derived Plaquesmentioning

confidence: 98%

The Microfibril Hypothesis of Glaucoma: Implications for Treatment of Elevated Intraocular Pressure

Kuchtey

2014

Journal of Ocular Pharmacology and Therapeutics

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“…Significantly, GAG-like deposits have been found in the juxtacanalicular connective tissue: in primary openangle glaucoma (a homogenous osmophilic materi al) [60] and in corticosteroid-induced glaucoma (a metachromatic amorphous and fibrous material) [61]. Scanning electron microscopic studies [62] indicate that an unknown substance on glaucomatous trabecular meshwork endothelial cell surfaces and/or in the intertrabecular matrix may play a key role in the pathogene sis of primary open-angle glaucoma.…”

Section: Functional Correlation Of Gags and The Outflow Pathwaysmentioning

confidence: 99%

Glycosaminoglycans and Outflow Pathways of the Eye and Brain

Knepper

McLone²

1985

Pediatr Neurosurg

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The etiology of the majority of defects of the outflow pathways of aqueous humor (glaucoma) and cerebrospinal fluid absorption (hydrocephalus) is unknown. A considerable amount of evidence indicates that glycosaminoglycans have a role in regulating fluid movement through connective tissues such as the trabecular meshwork of the eye and the arachnoid of the brain. Both the eye and the brain outflow pathways have hyaluronic acid and chondroitin sulfate within the filtration barrier. The physiological significance of glycosaminoglycans in the outflow pathways may be their ability to form highly viscous and elastic gel-like solutions that function as a selective biological gel filtration system, which maintains normal intraocular and intracranial pressure. We suggest that glycosaminoglycans may act to maintain the unidirectional character, low-flow fluid movement, and pressure gradient between the trabecular lamellae and the drainage channels of the eye and the brain. This review of the outflow pathways of the eye and the brain discusses the cell biology of glycosaminoglycans in regulating normal aqueous outflow and cerebrospinal fluid absorption.

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“…The predominant sites have been juxtacanicular region of the trabecular meshwork and the endothelial cells of the inner wall of Schlemm's canal. JCT lies close to the inner wall of the endothelium of the Schlemm's canal and is composed of loosely arranged extracellular matrix (ECM) into which JCT cells are embedded [4]. Abnormal regulation of aqueous flow through TM and JCT has been implicated in the elevation of IOP.…”

Section: Introductionmentioning

confidence: 99%

Elevated Intraocular Pressure induces Ultrastructural Changes in the Trabecular Meshwork

Vecino¹,

GaldósM²,

Bayón³

et al. 2015

J Cytol Histol

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The elevation of intraocular pressure (IOP) can be caused by the obstruction of flow in the trabecular meshwork and the age of the individuals has been pointed as one risk factor influencing in developing glaucoma. This study was designed to elucidate the morphological and ultrastructural changes in the trabecular meshwork of young adult Göttingen minipigs eyes after experimentally inducing a moderated chronic elevation of intraocular pressure lasting for over 14 months. The method used was cauterization of episcleral veins, located post-trabecular in the flow pathway and thus not affecting the cells located in the trabecular meshwork. The tissue was analysed using electron microscopy in control and experimental eyes. An increase in the amount of fibrillar material in the subendothelial region with a decreased optically empty spaces and an increase in rough endoplasmic reticulum (rER) were observed in the young experimental eyes. By experimentally increasing the post-trabecular resistance to the aqueous outflow, the present study showed that IOP elevation led to ultrastructural changes and thus concluded that changes in the trabecular meshwork can take place not only due to the advanced age, but by mechanical action on the cells as well.

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Electron microscopic studies on the trabecular meshwork in glaucoma simplex

Cited by 118 publications

References 7 publications

The Microfibril Hypothesis of Glaucoma: Implications for Treatment of Elevated Intraocular Pressure

The Microfibril Hypothesis of Glaucoma: Implications for Treatment of Elevated Intraocular Pressure

Glycosaminoglycans and Outflow Pathways of the Eye and Brain

Elevated Intraocular Pressure induces Ultrastructural Changes in the Trabecular Meshwork

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