Human Schlemm's canal cells express the endothelial adherens proteins, VE-cadherin and PECAM-1

Heimark, Ronald L.; Kaochar, Salma; Stamer, W. Daniel

doi:10.1076/ceyr.25.5.299.13495

Cited by 53 publications

(48 citation statements)

References 41 publications

(45 reference statements)

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“…(Heimark et al 2002;Chen et al 2005;Vittal et al 2005) A variety of other cell-surface receptors and cellcell interaction proteins are expressed by TM/SC cells. These include sarcoglycan β and ε, dystroglycan and sarcospan, which are members of the dystroglycan glycoprotein complex that can serve as a laminin receptor in some tissues.…”

Section: Cell-surface Ecm Receptors Of the Tmmentioning

confidence: 99%

Extracellular matrix in the trabecular meshwork

Acott

Kelley

2008

Experimental Eye Research

417

443

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The extracellular matrix (ECM) of the trabecular meshwork (TM) is thought to be important in regulating intraocular pressure (IOP) in both normal and glaucomatous eyes. IOP is regulated primarily by a fluid resistance to aqueous humor outflow. However, neither the exact site nor the identity of the normal resistance to aqueous humor outflow has been established. Whether the site and nature of the increased outflow resistance, which is associated with open-angle glaucoma, is the same or different from the normal resistance is also unclear.The ECMs of the TM beams, juxtacanalicular region (JCT) and Schlemm's canal (SC) inner wall are comprised of fibrillar and non-fibrillar collagens, elastin-containing microfibrils, matricellular and structural organizing proteins, glycosaminoglycans (GAGs) and proteoglycans. Both basement membranes and stromal ECM are present in the TM beams and JCT region. Cell adhesion proteins, cell surface ECM receptors and associated binding proteins are also present in the beams, JCT and SC inner wall region.The outflow pathway ECM is relatively dynamic, undergoing constant turnover and remodeling. Regulated changes in enzymes responsible for ECM degradation and biosynthetic replacement are observed. IOP homeostasis, triggered by pressure changes or mechanical stretching of the TM, appears to involve ECM turnover. Several cytokines, growth factors and drugs, which affect the outflow resistance, change ECM component expression, mRNA alternative splicing, cellular cytoskeletal organization or all of these. Changes in ECM associated with open-angle glaucoma have been identified.

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Section: Cell-surface Ecm Receptors Of the Tmmentioning

confidence: 99%

Extracellular matrix in the trabecular meshwork

Acott

Kelley

2008

Experimental Eye Research

417

443

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“…It has been postulated by several investigators (Epstein and Rohen, 1991;Alvarado et al, 1998;Brandt and O'Donnell, 1999;Underwood et al, 1999;Rao et al, 2001;Heimark et al, 2002) that instead of passing through the pores in the inner wall endothelium, a significant fraction of the aqueous humour passes through gaps between the tight junction strands of these cells. Ethier and Chan (Ethier and Chan, 2001) found that cationized ferritin perfused into enucleated human eyes acted to decreased outflow facility and was seen accumulating near junctions between inner wall endothelial cells.…”

Section: Pores As Possible Fixation Artifacts and The Possible Importmentioning

confidence: 99%

‘What controls aqueous humour outflow resistance?’

Johnson

2006

Experimental Eye Research

405

366

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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...

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“…22 Of note is that, among the cadherin family junctional genes being expressed, VEcadherin was not tested in these arrays, nor was PECAM, both reported to be expressed in SC cells in culture. 23,24 Fibulin 2, also reported in SC cells, 24,25 was also not tested in this array, but fibulin 1 was much higher in SC cells. The fibulins are interesting as an elastic component of the ECM and basement membrane.…”

Section: Resultsmentioning

confidence: 85%

“…Thus, our results are consistent with an endothelial identity of the SC cells. 5,23,24,28 One interesting question is what role chitinase family proteins play in the outflow pathway. Liton et al showed that the chitinase 3-like 1 gene was strongly overexpressed in TM cells relative to SC.…”

Section: Resultsmentioning

confidence: 99%

Differential Expression of Genes in Cells Cultured from Juxtacanalicular Trabecular Meshwork and Schlemm's Canal

Wang

Ying

Yue

2014

Journal of Ocular Pharmacology and Therapeutics

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Purpose: The purpose of this study was to distinguish differences in gene expression between cells cultured from the juxtacanalicular trabecular meshwork ( JCTM) and those from Schlemm's canal (SC), to gain clues to differences between those cell types, and to add to our baseline knowledge of gene expression differences in these cell types for later comparison between cells from nonprimary open-angle glaucoma (POAG) and POAG outflow tissues. Methods: A set of JCTM and SC cells was cultured from each of 2 donor eyes by an explant method, grown to passage 3, and frozen in liquid nitrogen. The cells were thawed, total RNA was extracted, and the probes made from total RNAs were hybridized to MICROMAX human cDNA microarray slides in 2 separate trials. Differentially expressed genes were analyzed using PubMed, Prosite, and IPA software, and the expression of several of the genes including intercellular adhesion molecule-1 (ICAM-1), tenascin, and b-spectrin was assessed by immunofluorescence. Results: Schlemm's canal cells differentially expressed ICAM-1, spectrin, complement, fibulin-1, and several genes consistent with an endothelial origin in both arrays, while the JCTM cells more often overexpressed genes consistent with contractile, matrix function, and neural character. At the same time, many genes highly expressed in the first array were not highly overexpressed in the second. One highly overexpressed gene in the JCTM in both arrays, that for heparan sulfate 3-O-sulfotransferase-1 precursor, is thought to be somewhat unique, and could affect the glycosaminoglycan functionality in the extracellular matrix (ECM). Conclusions: We found generally good agreement between the 2 array trials, but some contradictions as well. Many of the genes overexpressed in each cell type had been described in earlier work, but several were new. Tables of genes, grouped by cellular function, and the complete datasets are provided for the development of new hypotheses.

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Human Schlemm's canal cells express the endothelial adherens proteins, VE-cadherin and PECAM-1

Cited by 53 publications

References 41 publications

Extracellular matrix in the trabecular meshwork

Extracellular matrix in the trabecular meshwork

‘What controls aqueous humour outflow resistance?’

Differential Expression of Genes in Cells Cultured from Juxtacanalicular Trabecular Meshwork and Schlemm's Canal

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