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PubMed1981

The development of the trabecular meshwork and its abnormality in primary infantile glaucoma.

Tissue from ten eyes with infantile glaucoma and from 40 normal eyes of fetuses and infants without glaucoma were examined by light and electron microscopy. In normal development, the corneoscleral coat grows faster than the uveal tract during the last trimester, leading to a posterior migration of the ciliary body attachment from Schwalbe's line (5th month) to the scleral spur (9th month), and then to a location behind the scleral spur (postnatally). In infantile glaucoma, the insertion of the anterior ciliary body and iris overlaps the trabecular meshwork, similar to the late fetal position. The trabecular sheets are perforated, and there is no membrane over the surface of the trabecular meshwork. The trabecular beams are thicker than in normal infant eyes. There is both histologic and clinical evidence of traction on the iris root exerted by the thickened trabecular beams. These findings suggest that in congenital glaucoma the thickened beams had prevented the normal posterior migration of the ciliary body and iris root. This traction may compact the thickened trabecular beams, obstructing aqueous humor outflow. Release of the traction by an incision (goniotomy or trabeculotomy) of the thickened meshwork may relieve the obstruction. Of uncertain pathological significance is that there are no vacuoles in the endothelium of Schlemm's canal and there is a broad layer of collagen and amorphous material in the juxtacanalicular connective tissue. The ciliary processes are elongated inward, as if they were pulled by zonular traction (perhaps created by an enlarging diameter of the limbus with a fixed lens diameter).

Child↗
PubMed1998

Immunohistochemical distribution of type VI collagen in normal and glaucomatous human trabecular meshwork.

BACKGROUND: An abnormally increased presence of type VI collagen has been shown in the lamina cribrosa of patients with primary and secondary glaucoma. This study was undertaken to investigate the pattern of type VI collagen within the aqueous outflow structures of glaucoma patients. METHODS: Trabecular meshwork samples of eight normal donor eyes and trabeculectomy specimens of 21 patients with different types of glaucoma were processed for either cryo-sectioning or for paraffin embedding. Immunohistochemical staining was conducted by use of polyclonal rabbit antibodies against human collagen type VI. RESULTS: Immunoreactivity for type VI collagen was evident in the cores of all trabecular beams. The strongest staining was detected in the uveal region of the human trabecular meshwork. Immunohistochemical labelling for type VI collagen was not more pronounced in the aqueous outflow structures of glaucoma patients than in normal eyes. CONCLUSION: Collagen type VI is a ubiquitous structural component of the extracellular matrix in the human trabecular meshwork. However, type VI collagen does not appear to be of greater importance for the increased trabecular outflow resistance in glaucoma patients than in normal eyes.

Adolescent↗
PubMed1990

The effect of dexamethasone on glycosaminoglycans of human trabecular meshwork in perfusion organ culture.

The effect of dexamethasone treatment on glycosaminoglycans (GAG) in the human trabecular meshwork was studied by placing 20 pairs of eyes in perfusion organ culture. One eye received 550 nM dexamethasone in addition to culture medium; the fellow eye received culture medium only. 3H-glucosamine and 35S-sulfate were added to the medium for the final 48 hr of culture. The meshwork was then dissected, and the GAGs were isolated and subjected to sequential enzymatic degradation. Active labeling of hyaluronic acid, chondroitin sulfate, dermatan sulfate, keratan sulfate, and heparan sulfate was found in both control and steroid-treated eyes. Dexamethasone-treated eyes had an average 92% increase in the 3H-glucosamine incorporation rate in the undigestible GAG residue fraction after 14-21 days treatment (20.6% versus 10.7%, P = 0.03). This change was not apparent in eyes treated for 7 days. In this preliminary study, dexamethasone appeared to cause a time-dependent increase in the undigestible GAG incorporation profile in human trabecular meshwork.

Adult↗
PubMed1984

Neuron-specific enolase-containing cells in the rhesus monkey trabecular meshwork.

Neuron-specific enolase (NSE) localizes immunohistochemically to a discontinuous band of cell clusters in the trabecular meshwork of the anterior segment of the rhesus monkey eye. To date, this enolase isomer has been found exclusively in neurons or in cells of the diffuse neuroendocrine system. On this basis, its presence provides presumptive evidence for neuroregulatory cells in the primate trabecular meshwork.

Animals↗
PubMed1993

[An electron microscopic histochemical study on the localization of sialic acids in human trabecular meshwork].

The localization of sialic acids in human trabecular meshworks of normal eyes, primary open angle glaucoma (POAG) eyes, congenital glaucoma eyes, and juvenile glaucoma eyes was investigated using biotinyl lectin (LPA, SSA, MAM) and avidin-gold electron microscopic histochemistry. Gold particles were detectable in fine fibrils underneath Schlemm's canal and collagen fibers of normal, POAG, congenital glaucoma, and juvenile glaucoma eyes equally. Many gold particles were detected especially in fine fibrils and basal membrane (compact tissue) 3 microns underneath Schlemm's canal. The present study indicated that extracellular matrices of congenital glaucoma and juvenile glaucoma contained sialic acids and that this may be related to the ocular hypertension of these diseases.

Adult↗
PubMed2002

Confocal microscopic examination of trabecular meshwork removed during ab externo trabeculectomy.

AIMS: The aim of the ab externo trabeculectomy (AET) is to remove the external portion of the trabecular meshwork (ETM) responsible for the main aqueous outflow resistance in glaucoma patients, with no opening of the anterior chamber. ETM characteristics were evaluated with a confocal microscope. METHODS: A prospective comparative observational case series was performed in 60 consecutive medically treated patients with primary open angle glaucoma and eight postmortem normal donors' eyes that underwent AET. Once deroofing the Schlemm' s canal (SC), a deeper dissection led to removal of a coherent membrane (ETM) which allowed satisfactory aqueous egress through the remaining intact internal trabecular meshwork (TM) layers. After fixation with acetone and immunostaining with anti-vimentin antibody, ETM were analysed with a confocal microscope. RESULTS: Glaucomatous ETM (mean thickness: 29.5 (7.6) micro m) were characterised by a severe paucicellularity compared with the controls (respectively 37.3 (9.7) cells/area and 167.5 (24.9) cells/area, p<10(-4)). ETM analysis showed involvement of both cribriform and corneoscleral layers. ETM cell density was significantly decreased in case of preoperative fluorometholone instillation. CONCLUSION: Paucicellularity of glaucomatous TM is confirmed by this original technique. Structural characteristics of the ETM, whose removal allows satisfactory aqueous egress, suggest that aqueous outflow resistance not only involves inner wall of SC and juxtacanalicular meshwork but also corneoscleral trabecular layers.

Adult↗
PubMed1994

[Protein profiles of normal and organ-cultured human trabecular meshwork].

We determined the protein profiles of the trabecular meshwork (TM) obtained from 14 normal human eyes from individuals of various ages (53 to 76 years) using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and a highly sensitive silver staining technique, which yields 50-100 times greater sensitivity than is achieved with Coomassie Blue. Over 30 protein bands varying in molecular weight from 16,000 to 250,000 were consistently visible, regardless of donor age. Protein profiles of one-eighth human TM obtained from each eye showed a same pattern and those of one-eight organ-cultured human TM during 4 weeks also indicated a same pattern. Protein profiles of the TM from normal human eyes of various ages shared a number of similarities. Protein profiles of the TM, peripheral cornea, limbal sclera, iris, and ciliary body from a control donor were similar, although several polypeptide bands were unique to each structure.

Aged↗
PubMed1989

Kinetics of phagocytosis in trabecular meshwork cells. Flow cytometry and morphometry.

Confluent human trabecular meshwork (HTM) cells from three different donors and at various stages of serial passage were fed fluorescein-labeled polystyrene beads. Phagocytosis was monitored for up to 6 days using flow cytometry, fluorescence microscopy, and morphometric calculations from comprehensive electron microscopic observations at key time points. During the first 4 hr after initiation of phagocytosis, the confluent endothelial monolayer lost its cohesiveness and became segregated into separate cells. During the first 3 days the cells underwent marked and progressive changes in shape and size. After 4 days, some cells detached from the dish, as necrotic debris and degenerative changes appeared. The kinetics of phagocytosis in this stable, confluent monolayer showed that recruitment (the percentage of cells which had ingested at least one bead) proceeded semilogarithmically, with 50% of the cells recruited by 8 hr and 97% by 96 hr. The time course of phagocytosis (ie, the average number of beads phagocytosed per cell) is described by a sigmoidlike curve, reaching half-maximum at 40 hr and maximum (about 500 beads per cell) at 96 hr. The rate of uptake (ie, the first derivative of the average number of beads per cell) reached a peak (nine beads per cell per hr) at 24 hr and then decelerated slowly over the next 5 days. Cytochalasin B treatment, as a control, reduced phagocytosis by approximately 70%. Flow cytometry, when combined with electron microscopy, should provide a useful tool to examine phagocytosis in HTM cells exposed to steroids and other hormones and drugs.

Adult↗
PubMed1994

Localization of elastin in the normal and glaucomatous human trabecular meshwork.

PURPOSE: The extracellular materials (ECMs) in the trabecular meshwork (TM) are thought to play a crucial role in aqueous outflow resistance. Immunohistochemical localization of elastin, one of the major ECMs in the normal and glaucomatous human TM, was examined ultrastructurally. METHODS: Eight normal eye bank eyes and 16 trabeculectomy specimens of primary open angle glaucoma (POAG, 11 eyes from 8 cases), congenital glaucoma (2 eyes from 1 case), and juvenile glaucoma (3 eyes from 2 cases) were embedded in Lowicryl K4M at low temperature. The distribution of elastin was studied by the protein A-gold technique. RESULTS: In normals, the gold particles indicating the antigenic sites for elastin existed mainly in the central amorphous element of the elastic-like fibers, and a few gold particles were observed within the area containing fine granular-like material and fine fibrillar-like material. No labeling was observed in cellular materials or other ECMs. In congenital and juvenile glaucoma, labeling was similar to that observed in normals. In POAG specimens compared to normals, there was an increased amount of elastin-bound immunogold particles along the inner canal endothelium. The increased gold particles, which did not have a fibrillar arrangement and were not enclosed by electron-dense microfibrils, were found within the area containing fine fibrillar-like material. However, labeling within the elastic-like fibers was similar to that observed in normals. CONCLUSIONS: Under electron microscopy, elastin could be localized in the normal and glaucomatous human TM. The results of this investigation suggest that elastin may play an important role in the etiology of POAG.

Adult↗
PubMed2005

Changes in gene expression by trabecular meshwork cells in response to mechanical stretching.

PURPOSE: Trabecular meshwork (TM) cells appear to sense changes in intraocular pressure (IOP) as mechanical stretching. In response, they make homeostatic corrections in the aqueous humor outflow resistance, partially by increasing extracellular matrix (ECM) turnover initiated by the matrix metalloproteinases. To understand this homeostatic adjustment process further, studies were conducted to evaluate changes in TM gene expression that occur in response to mechanical stretching. METHODS: Porcine TM cells were subjected to sustained mechanical stretching, and RNA was isolated after 12, 24, or 48 hours. Changes in gene expression were evaluated with microarrays containing approximately 8000 cDNAs. Select mRNA changes were then compared by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Western immunoblots were used to determine whether some of these changes were associated with changes in protein levels. RESULTS: On the microarrays, 126 genes were significantly upregulated, and 29 genes were significantly downregulated at one or more time points, according to very conservative statistical and biological criteria. Of the genes that changed, several ECM regulatory genes, cytoskeletal-regulatory genes, signal-transduction genes, and stress-response genes were notable. These included several proteoglycans and matricellular ECM proteins composed of common repetitive binding domains. The results of analysis of mRNA changes in more than 20 selected genes by qRT-PCR supported the findings in the microarray analysis. Western immunoblots of several proteins demonstrated protein level changes associated with changes in the level of mRNA. CONCLUSIONS: The expression of a variety of TM genes is significantly affected by mechanical stretching. These include several ECM proteins that contain multiple binding sites and may serve organizational roles in the TM. Several proteins that could contribute to the homeostatic modification of aqueous humor outflow resistance are also upregulated or downregulated.

Animals↗
PubMed2003

Gene expression in the trabecular meshwork and the influence of intraocular pressure.

The trabecular meshwork (TM) tissue is responsible for maintaining the physiologic intraocular pressure (IOP) of the ocular globe. To perform this function the TM must rely on a variety of mechanisms. These mechanisms, acting either independently or in a coordinated manner, are governed by the expression of TM genes. Expression profiles of TM from adult intact tissue and infant cultured cells revealed the high level of diversity of the TM transcriptome, with only about 1% of its genes represented by more than 4 clones in any of the libraries. The profiles also revealed genes whose presence is associated with previously undescribed TM functions such the one that protects the TM tissue against calcification. These findings support the existence of numerous regulatory mechanisms in the TM and may help explaining the low percentage of glaucoma patients associated with each mutated glaucoma gene. Failure to maintain a physiological pressure can result in elevated IOP, a condition often associated with the development of glaucoma. Experimentally, different time-periods of an elevated pressure insult lead to the altered expression of distinct sets of genes. Thus, the ability of the TM to respond to mechanical and biochemical insults is possibly driven by induction or repression of a number of genes that, most likely, are different from those involved in regulation of normal IOP. None of the genes currently linked to glaucoma was present in the expression profile libraries whereas their expression in the TM was highly induced by effectors known to be causative of glaucomatous conditions. This analysis leads to the speculation that glaucoma candidate genes might be more related to genes responding to insults than to those involved in the maintenance of normal TM physiology. A recent study implicating the common stress mediator NF-kappaB in glaucoma would support this notion. Future library profiles utilizing distinct RNA sources together with differential expression studies between normal and glaucoma-triggering conditions and individual characterization of selected genes will help elucidate the relevant mechanisms for the regulation of IOP.

Gene Expression↗
PubMed1981

Effect of iodoacetamide perfusion on outflow facility and metabolism of the trabecular meshwork.

Freshly enucleated eyes were quantitatively perfused via the anterior chamber with varying dosages of iodoacetamide at constant pressure. Iodoacetamide caused a significant increase in facility of outflow in a dose-response manner in calf and monkey eyes. Almost complete inhibition of glycolysis in the calf trabecular meshwork was produced by a dosage of iodoacetamide that was too low to appreciably alter the facility. A similar response was produced by a higher dosage, which did significantly increase the facility. Our results, taken together with what is known of the properties of iodoacetamide, suggest that cellular sulfhydryl groups may be involved in a mechanism for aqueous flow through the trabecular meshwork and that iodoacetamide probably acts directly on cellular permeability rather than by inhibition of glycolysis or interference with the production of energy in the trabecular meshwork.

Animals↗
PubMed2006

CB1 cannabinoid receptor-mediated changes of trabecular meshwork cellular properties.

PURPOSE: To evaluate the roles of CB1 cannabinoid receptors in cellular functions of trabecular meshwork (TM) cells, including cell migration, adhesion, morphology and cytoskeleton changes. METHODS: Noladin ether, a selective CB1 receptor agonist, and SR141716A, a selective CB1 receptor antagonist, were used to characterize the cellular functions of cultured porcine TM cells. Fluorescence assisted transmigration invasion and motility assays (FATIMA) were conducted to study TM cell migration using soluble fibronectin as a chemoattractant. Wound healing assays were used to further study TM cell migration. Standard cell adhesion assays of TM cells were performed on fibronectin-coated plates. In morphological studies, Alexafluor 488-labeled phalloidin staining was used to examine actin filaments, and immunocytochemistry using anti-paxillin antibodies was used to detect focal adhesions. RESULTS: In cell migration assays, CB1 agonist noladin ether at nanomolar ranges led to a concentration-dependent inhibition of migration of TM cells toward soluble fibronectin. CB1 antagonist SR141716A antagonized noladin ether-induced inhibition of migration of TM cells. In addition, noladin ether caused a delay in wound healing of confluent trabecular meshwork monolayers and this effect of noladin ether was antagonized by SR141716A. In cell adhesion assays, noladin ether treatment led to a moderate, but significant decrease of adhesion of TM cells to fibronectin-coated surface. This effect of noladin ether was concentration-dependent, and was antagonized by SR141716A. In morphological studies, noladin ether treatment caused rounding of TM cells in contrast to well-spread control TM cells. In addition, there was a reduction and fragmentation of actin stress fibers stained with Alexafluor 488-labeled phalloidin and a decrease of focal adhesions detected with an anti-paxillin antibody. CONCLUSIONS: Noladin ether modulates the migration, adhesion, morphology, and actin cytoskeleton of TM cells. These effects of noladin ether are mediated through TM cell CB1 cannabinoid receptors.

Actin Cytoskeleton↗
PubMed1977

Particulate phagocytosis by trabecular meshwork endothelium.

We studied the phagocytic response in the trabecular meshwork of rabbits to the debris released by photocoagulation of the iris. Four cell types exhibited phagocytosis: native meshwork endothelium, histiocytic macrophages, polymorphonuclear leukocytes and corneal endothelial cells. Nienty days after the photocoagulation both the lining cells and the trabecular beams of the meshwork had returned to normal.

Animals↗
PubMed1993

Corticosteroid treatment and trabecular meshwork proteases in cell and organ culture supernatants.

Steroid-induced glaucoma is believed to result from increased aqueous outflow resistance and evidence suggests that this is the result of an excess accumulation of extracellular matrix components. This accumulation could result from an imbalance in the natural turnover of these components. We have investigated the effect of corticosteroid treatment of trabecular meshwork (TM) organ and cell cultures on the extracellular activities of the matrix metalloproteinases and plasminogen activators. We find that corticosteroid treatment results in decreased extracellular activity of stromelysin and tissue plasminogen activator in trabecular meshwork cell culture, and decreased 92 kDa collagenase IV, stromelysin, and tissue plasminogen activator in trabecular meshwork organ culture. These data suggest that decreased levels of proteolytic activities could account, in part, for the accumulation of some extracellular matrix components and be a contributing mechanism in steroid-induced glaucoma.

Cells, Cultured↗
PubMed1989

Does pigmentation affect the trabecular meshwork?

Pigment has been associated with glaucoma in pigment dispersion syndrome and in intraocular lens-associated pigment dispersion. Human eyes with segmental pigmentation of the trabecular meshwork may provide a controlled model to study the effects of pigment on the meshwork. Nine normal human eye bank eyes with segmental pigmentation of the trabecular meshwork were examined for pigment-associated differences in trabecular cellularity or morphology. Cellularity was examined with four methods: cells per histologic section, cells per length of tissue, cells per overall area, and cells per solid tissue. The simplest method, cells per histologic section, gave results equivalent to the other methods. No differences in cellularity or morphology were found between pigmented and nonpigmented areas.

Adult↗
PubMed1991

Synthesis of a thrombospondin-like cytoadhesion molecule by cells of the trabecular meshwork.

Thrombospondin is a large extracellular-matrix protein that is released by smooth muscle cells and platelets and is distributed widely in mammalian brain. By using western blotting with a monoclonal antibody against the calcium-binding domain of thrombospondin, the authors detected a 180-kD glycated polypeptide in the trabecular meshwork tissue of normal human and porcine eyes. The epitope-bearing polypeptide was soluble in sodium dodecylsulfate/urea (SDS/urea), and apparently it was stabilized in part by disulfide bonding to the Triton X-100 and SDS/urea-insoluble pellet of this tissue. Treatment of the insoluble matrix with beta-mercaptoethanol led to an enriched extraction of the approximately 160-kD form of thrombospondin. On immunohistochemical study, the thrombospondin antibody also reacted positively with the extracellular matrix and intracellular structures of trabecular cells in primary monolayer culture. This suggested that the presence of thrombospondin in the trabecular meshwork was probably due to local synthesis. These findings are relevant to the establishment of a model in vitro for assessment of adhesion of trabecular cells. Because thrombospondin is a cell-substrate adhesion molecule, its role in the loss of cellularity that occurs in the trabecular meshwork of the aging eye and in eyes with primary open-angle glaucoma is worthy of further investigation.

Adult↗