Juxtacanalicular Tissue in Primary Open Angle Glaucoma and in Nonglaucomatous Normals

Alvarado, Jorge A.; Yun, Andersen J.; Murphy, Collin

doi:10.1001/archopht.1986.01050220111038

Cited by 59 publications

(31 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The increase in the intraocular pressure (IOP) is caused by an enhanced outfl ow resistance across the trabecular meshwork (TM) [1][2][3] . The histopathological changes observed in the TM in glucocorticoid-treated eyes bore some similarities with those described in eyes affl icted with primary open angle glaucoma (POAG) [4][5][6][7][8][9] .…”

Section: Introductionmentioning

confidence: 69%

Myocilin Gene Expression in the Trabecular Meshwork of Rats in a Steroid-Induced Ocular Hypertension Model

Sawaguchi

Nakamura

et al. 2005

Ophthalmic Res

View full text Add to dashboard Cite

Purpose: To investigate the expression pattern of myocilin in the trabecular meshwork of normal and dexamethasone-induced ocular hypertensive rat eyes. Materials and Methods: An ocular hypertension model was generated by application of topical dexamethasone to rat eyes 4 times daily for 1, 2, and 4 weeks. Age-matched untreated eyes served as controls. The intraocular pressure (IOP) was monitored by electronic Tono-pen under anesthesia. The protein and mRNA levels of myocilin in the trabecular meshwork and endothelial lining of Schlemm’s canal were investigated by immunohistochemistry and in situ hybridization, respectively. For semiquantitative evaluation, areas with positive staining were analyzed by a computer-assisted image-processing system with NIH software. Results: The IOP in rat eyes was elevated after 2 weeks of topical dexamethasone treatment. Despite the IOP elevation, the protein and mRNA levels of myocilin in the trabecular meshwork and around Schlemm’s canal in the steroid-treated eyes were not different from those of controls. Conclusion: No discernible changes in myocilin expression in the chamber angle indicate that myocilin may not be directly linked to ocular hypertension, at least not in rat eyes after relatively short-term steroid application.

show abstract

Section: Introductionmentioning

confidence: 69%

Myocilin Gene Expression in the Trabecular Meshwork of Rats in a Steroid-Induced Ocular Hypertension Model

Sawaguchi

Nakamura

et al. 2005

Ophthalmic Res

View full text Add to dashboard Cite

show abstract

“…It thus followed that either this region was filled with an extracellular matrix gel that was poorly visualized using conventional TEM techniques, or, that this region was not the primary site of outflow resistance. The age-related accumulation of 'plaque-like material' in this region that is enhanced in glaucomatous would have no influence on this conclusion (Alvarado et al, 1986;Murphy et al, 1992). …”

Section: The Juxtacanalicular Connective Tissue (Jct)mentioning

confidence: 98%

“…The extracellular matrix components include collagen types I, III, IV, V and VI (but not type II), (Lütjen-Drecoll et al, 1989;Marshall et al, 1990;Marshall et al, 1991) elastin, (Gong et al, 1989) laminin, (Marshall et al, 1990) fibronectin, (Gong et al, 1996) and glycosaminoglycans, particularly dermatan sulfate, chondroitin sulfate and hyaluronic acid (Gong et al, 1996). With aging, this region shows an accumulation of structures called plaques (Lütjen-Drecoll et al, 1981;Alvarado et al, 1986). In glaucoma, there appears to be an increased age-related accumulation of plaque material, although this accumulation has little hydrodynamic consequence, as mentioned below.…”

Section: The Inner Wall Region Of Schlemm's Canalmentioning

confidence: 99%

‘What controls aqueous humour outflow resistance?’

Johnson

2006

Experimental Eye Research

403

366

View full text Add to dashboard Cite

The bulk of aqueous humour outflow resistance is generated in or near the inner wall endothelium of Schlemm's canal in normal eyes, and probably also in glaucomatous eyes. Fluid flow through this region is controlled by the location of the giant vacuoles and pores found in cells of the endothelium of Schlemm's canal, but the flow resistance itself is more likely generated either in the extracellular matrix of the juxtacanalicular connective tissue or the basement membrane of Schlemm's canal. Future studies utilizing in vitro perfusion studies of inner wall endothelial cells may give insights into the process by which vacuoles and pores form in this unique endothelium and why inner wall pore density is greatly reduced in glaucoma. Keywordsglaucoma; Schlemm's canal; hydraulic conductivity It has been recognized for more that 130 years that the elevated pressure characteristic of primary open-angle glaucoma arises due to an increased resistance to the outflow of aqueous humour from the eye. (Leber, 1873) However, a conclusive determination of where in the outflow pathways this elevated outflow resistance is generated has been elusive. Surprisingly, the locus of aqueous humour outflow resistance in the normal eye has also been not been unequivocally determined.Seidel (1921) using light microscopy, stated 'that the inner wall of Schlemm's canal stand in open communication with the anterior chamber, and that the aqueous humour directly washes around the inner wall endothelium of Schlemm's canal and is only separated from the lumen of Schlemm's canal by a thin, outer membrane'. Our view is little different today. The locus of outflow resistance, both in the normal eye and the glaucomatous eye, is thought to arise either in the endothelial lining of Schlemm's canal, or very near to this location. In this article, current thoughts on where that flow resistance might be generated are reviewed.There are a number of excellent review articles (Tripathi, 1974a,b;Bill, 1975;Bill and Mäepea, 1994;Gong et al., 1996;Johnson and Erickson, 2000;Ethier, 2002) that describe the detailed morphology and physiology of the aqueous outflow pathway. In this review, the evidence that leads to the conclusion that the inner wall region is responsible for the bulk of aqueous humour outflow resistance is first presented. Then, attention is focused on those proximal aspects of this pathway that are nearest to the endothelial linings of Schlemm's canal, and the transport characteristics of these structures.The bulk of the aqueous humour flows out of the anterior chamber of the eye through the conventional aqueous outflow pathway comprised of the trabecular meshwork, the juxtacanalicular connective tissue, the endothelial lining of Schlemm's canal, Schlemm's canal itself, the collecting channels and aqueous veins, and then finally drains into the episcleral NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript venous system, rejoining the blood from whence it came (in this review, the juxtacanalicular...

show abstract

“…S1P and LPA activity are mediated through G-protein coupled receptors specific for each molecule. LPA binds to four receptor subtypes (LPA 1-4 formerly Edg 2, 4, 7, p24a/GPR23), whereas S1P binds specifically to a group of five receptor subtypes (S1P receptors1-5, formerly know as Edg1, 3,5,6,8). Not surprisingly, LPA and S1P receptor subtypes are differentially expressed in tissues, likely in alignment with specific functional requirements of each tissue.…”

Section: Lysophospholipidsmentioning

confidence: 99%

“…Measured by tonography, Grant showed in vivo that glaucomatous eyes have reduced outflow through the conventional tract [6]. Accompanying decreased outflow facility are fewer trabecular meshwork cells in the inner meshwork and more plaque material in the juxtacanalicular tissue (JCT) of the conventional outflow tract [7][8][9]. Since the conventional outflow pathway is pressure-sensitive and accounts for the majority of aqueous humor outflow (70-90% of total), it is not surprising that cellular dysfunction impacts IOP [10,11].…”

Section: Introduction Epidemiology and Pathophysiology Of Glaucomamentioning

confidence: 99%

Endogenous bioactive lipids and the regulation of conventional outflow facility

Wan

Woodward

Stamer

2008

Expert Review of Ophthalmology

View full text Add to dashboard Cite

SummaryPerturbation of paracrine signaling within the human conventional outflow pathway influences tissue homeostasis and outflow function. For example, exogenous introduction of the bioactive lipids, sphingosine-1-phosphate, anandamide or prostaglandin F 2α , to conventional outflow tissues alters the rate of drainage of aqueous humor through the trabecular meshwork, and into Schlemm's canal. This review summarizes recent data that characterizes endogenous bioactive lipids, their receptors and associated signaling partners in the conventional outflow tract. We also discuss the potential of targeting such signaling pathways as a strategy for the development of therapeutics to treat ocular hypertension and glaucoma.

show abstract

Juxtacanalicular Tissue in Primary Open Angle Glaucoma and in Nonglaucomatous Normals

Cited by 59 publications

References 12 publications

Myocilin Gene Expression in the Trabecular Meshwork of Rats in a Steroid-Induced Ocular Hypertension Model

Myocilin Gene Expression in the Trabecular Meshwork of Rats in a Steroid-Induced Ocular Hypertension Model

‘What controls aqueous humour outflow resistance?’

Endogenous bioactive lipids and the regulation of conventional outflow facility

Contact Info

Product

Resources

About