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PubMed1986

Innervation of trabecular meshwork.

The innervation of the trabecular meshwork of the anterior chamber angle in monkey eyes was studied by transmission and scanning electron microscopy. According to the transmission electron microscopic examination, the nerve terminals in the trabecular meshwork mostly contained dense core vesicles after treatment with 5-hydroxydopamine and thus were identified as the adrenergic nerve terminals. Regarding the mode of ending of the nerve terminals in the trabecular meshwork, it was divided into three types from the positional relationship of the nerve terminals with the endothelial cells in the trabecular meshwork. Type I nerve terminals are naked and they form synaptic contact with endothelial cells of the trabecular sheets of the uveal and corneoscleral meshwork. Type II nerve terminals are located in the trabecular sheets of the uveal and corneoscleral meshwork and in the endothelial meshwork, and partly surrounded by the Schwann cell processes. This type of nerve terminals end as free terminals without a constant relation to endothelial cells of the trabecular meshwork. Type III nerve terminals usually not surrounded by the Schwann cell processes are observed on the free surface of the endothelium of the trabecular sheets facing the aqueous humor. The incidence of these three types of nerve terminals was the highest in type II followed by type III. Type I nerve terminals were very rare. When the morphological characteristics of the trabecular meshwork are considered, the transmitter released from type II and type III nerve terminals enter the aqueous humor and perhaps affects the aqueous outflow area to control the intraocular pressure, as judged from the flow of aqueous humor.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Expression of HLA class I and II antigens on cells of the human trabecular meshwork.

Human corneoscleral tissue containing trabecular meshwork and cultured human trabecular cells were examined for HLA-ABC (class I) and HLA-DR (class II) antigens of the major histocompatibility complex using an indirect immunofluorescence assay. Class I antigens were detected in the trabecular meshwork on frozen sections and on cultured trabecular cells. Class II antigens were constitutively expressed on some, but not all, cells within the trabecular meshwork. Many more cells could be induced to express class II antigens by pre-incubation in human gamma interferon. Cultured trabecular cells did not express class II antigens constitutively, but expression could be induced by gamma interferon. This study suggests that, in addition to Langerhans' cells at the limbus, other cell types within the anterior segment express major histocompatibility complex-encoded class II antigens either constitutively or inducibly. These cells may be important for the initiation and regulation of ocular immunity.

Adult↗
PubMed1999

Functional morphology of the trabecular meshwork in primate eyes.

The trabecular meshwork forms most of the resistance to aqueous humor outflow needed for maintenance of a pressure gradient between intraocular pressure of approximately 17 mmHg and venous pressure of approximately 10 mmHg. The composition of the extracellular material in the subendothelial or cribriform layer seems to be mainly responsible for outflow resistance. The aqueous humor pathways through the subendothelial layer can be influenced by ciliary muscle contraction and presumably also by contractile elements recently found both in trabecular meshwork and scleral spur. Pharmacologically induced disconnection of inner wall and cribriform cells leads to wash out of extracellular material through breaks of the endothelial lining of Schlemm's canal and to increase of outflow facility. In glaucomatous eyes the resistance to aqueous humor outflow is increased due to an increase in different forms of extracellular material deposited within the cribriform layer. The amount of this newly developed extracellular material is correlated with loss of axons in the optic nerve, indicating that a common factor is responsible for both changes. To investigate the effect of various factors on the biology of trabecular cells monolayer cultures derived from cribriform and corneoscleral trabecular meshwork have been established. The two cell lines can be differentiated because cribriform cells in vivo as in vitro stain for alphabeta-crystallin whereas the corneoscleral cells remain unstained. The effect of TGFbeta, a growth factor increased in aqueous humor of glaucomatous eyes and glycocorticoids on trabecular meshwork cells show typical changes in formation of extracellular matrix components and of stress proteins. Dexamethasone and oxidative damage also lead to increase of trabecular meshwork inducible glucocorticoid response (TIGR) protein. A mutation of the TIGR-gene family has recently been found in families with juvenile and chronic simple glaucoma. Future research has to clarify the significance of these genetic factors for the pathophysiology of glaucoma and the role of trabecular cell activity in this respect.

Animals↗
PubMed1984

Nerve fibers in trabecular meshwork surface.

The trabecular meshwork surface in the Japanese monkey eye was observed by scanning electron microscopy. Many varicose nerve fibers were recognized in the anterior surface of the trabecular sheets and in the intertrabecular space facing the anterior chamber. The nerve fibers often branched and thus formed a loose-meshed plexus. These varicose nerve fibers were identified by ultrastructural studies after the pretreatment of one animal with 5-hydroxydopamine as an adrenergic agent. Most nerve fibers terminated as free endings without a constant relationship to the endothelial cells of the trabecular sheets. Although the physiological significance of such nerve fibers is not clear, they probably release a transmitter (noradrenaline) into the aqueous humor and have an influence on the aqueous outflow area.

Animals↗
PubMed1986

Establishment of calf trabecular meshwork cell cultures.

Trabecular meshwork cell cultures have been grown from excised calf aqueous outflow pathway tissue using two different methods. In one method, tissue explants were placed directly in culture dishes and primary cultures were established by those cells migrating from the tissue. In the second method, a cell suspension was generated by incubating trabecular tissue strips with 0.1% pronase, and the washed cells were used to seed primary cultures. The cell cultures generated by each method appeared to progress through morphological and biochemical changes characteristic of the cell type, although at different respective rates. Comparisons of the cell morphologies, biosynthetic activities, and growth characteristics of the respective subcultures suggested that similar cell populations were obtained by each method. These studies further suggested that sufficient quantities of calf trabecular cells could be grown in culture to permit biochemical and pharmacological studies of trabecular-cell metabolism.

Animals↗
PubMed1995

[Effect of RU486 on metabolism of glycosaminoglycans in the cultured calf trabecular meshwork cells].

The trabecular meshwork from newborn bovine eyes was used for cell culture and subculture to the third passage. Then the concentrations of RU486, a corticosteroid antagonist, in the medium were made to be 50, 100 and 200 micrograms/ml and 3H-glycosamine was introduced as the radioactive precursor. After extraction and purification, an aliquot of glycosaminoglycans (GAGs) was used for cellulose acetate electrophoresis, sequential degradation by different enzymes and radioactivity determination by scintillation counting to determine the total amount of GAGs and the amounts of constituents, such as hyaluronic acid (HA), etc. In the control group, the total amount of GAGs was 980 DPM/micrograms cell prot (disintegration per minute/micrograms cell protein) and HA accounted for 17.8%, while in the medium of 50 micrograms/ml and 100 micrograms/ml RU486, HA was increased to 50.1% and 46.1%, respectively. In the medium of 200 micrograms/ml RU486, the total amount of GAGs was decreased to 695 DPM/micrograms cell prot. The results were consistent with the theory of pharmacology and pharmacodynamics. It is possible that the corticosteroid antagonist can be used to reverse the pathogenesis of primary open-angle glaucoma.

Animals↗
PubMed2002

Myocilin is associated with mitochondria in human trabecular meshwork cells.

The trabecular meshwork (TM) is a specialized tissue located at the chamber angle of the eye next to the cornea. This tissue is believed to be responsible for regulation of the aqueous humor outflow and control of the intraocular pressure (IOP). Alterations in functions of the TM may lead to IOP elevation and development of glaucoma, a major cause of blindness. The myocilin gene has recently been directly linked to open-angle glaucomas. The gene product was originally identified as a protein inducible in TM cells by treatment with glucocorticoids such as dexamethasone (DEX) and termed TIGR (TM inducible-glucocorticoid response). The exact nature and function of the myocilin protein so far still remain elusive. In this study, myocilin was localized to the perinuclear region of both DEX-treated and control TM cells. Its distribution overlapped considerably with that of mitochondria. Subcellular fractionation and Western blot analyses suggested a rather extensive association of myocilin with mitochondria. The DEX-treated TM cells were found to undergo apoptosis, when exposed to anti-Fas antibody, to a significantly higher degree than the untreated control cells. It appears that the TM cell integrity remains intact after DEX treatment. However, the induced myocilin or myocilin-mitochondria association seems to render the cells more susceptible to a second stress or challenge. This vulnerability may be the basis that ultimately leads to pathological consequences.

Antibodies↗
PubMed2004

Extracellular myocilin affects activity of human trabecular meshwork cells.

The trabecular meshwork (TM), a specialized eye tissue, is a major site for regulation of the aqueous humor outflow. Malfunctioning of this tissue is believed to be responsible for development of glaucoma, a blinding disease. Myocilin is a gene linked to the most common form of glaucoma. The protein product has been localized to both intra and extracellular sites, but its function still remains unclear. This study was to determine whether extracellular myocilin presented in the matrix affects adhesion, morphology, and migratory and phagocytic activities of human TM cells in culture. Cell adhesion assays indicated that TM cells, while adhering readily on fibronectin, failed to attach on recombinant myocilin purified from bacterial cultures. Adhesion on fibronectin was also compromised by myocilin in a dose dependent manner. Myocilin in addition triggered TM cells to assume a stellate appearance with broad cell bodies and microspikes. Loss of actin stress fibers and focal adhesions was observed. TM cell migration on fibronectin/myocilin to scratched wounds was reduced compared to fibronectin controls. Myocilin, however, had little impact on phagocytic activities of TM cells. Cell attachment on fibronectin and migration of corneal fibroblasts, a control cell type, were not altered by myocilin. These results demonstrate that extracellular myocilin elicits anti-adhesive and counter-migratory effects on TM cells. Myocilin in the matrix of tissues could be exerting a similar influence on TM cells in vivo, impacting the flexibility and resilience required for maintenance of the normal aqueous outflow.

Actins↗
PubMed1995

Na-K-Cl cotransport regulates intracellular volume and monolayer permeability of trabecular meshwork cells.

The trabecular meshwork (TM) of the eye plays a critical role in modulating intraocular pressure (IOP) through regulation of aqueous humor outflow, although the underlying mechanisms remain unknown. Ethacrynic acid, an agent known to inhibit Na-K-Cl cotransport of a number of cell types, recently has been reported to increase aqueous outflow and lower IOP through an unknown effect on the TM. In vascular endothelial cells and a variety of other cell types, the Na-K-Cl cotransporter functions to regulate intracellular volume. The present study was conducted to evaluate TM cells for the presence of Na-K-Cl cotransport activity and to test the hypothesis that modulation of cotransport activity alters intracellular volume and, consequently, permeability of the TM. We demonstrate here that bovine and human TM cells exhibit robust Na-K-Cl cotransport activity that is inhibited by bumetanide and by ethacrynic acid. Our studies also show that TM cell Na-K-Cl cotransport is modulated by a variety of hormones and neurotransmitters. Inhibition of the cotransporter either by bumetanide, ethacrynic acid, or inhibitory hormones reduces TM intracellular volume, whereas stimulatory hormones increase cell volume. In addition, shrinkage of the cells by hypertonic media stimulates cotransport activity and initiates a subsequent regulatory volume increase. Permeability of TM cell monolayers, assessed as transmonolayer flux of [14C]sucrose, is increased by hypertonicity-induced cell shrinkage and by bumetanide. These findings suggest that Na-K-Cl cotransport of TM cells is of central importance to regulation of intracellular volume and TM permeability. Defects of Na-K-Cl cotransport may underlie the pathophysiology of glaucoma.

Animals↗
PubMed2006

Effects of endothelin-1 and flunarizine on human trabecular meshwork cell contraction.

Trabecular meshwork (TM) cells are now considered to play an active role in the aqueous outflow mechanism because they exhibit smooth muscle-like contractile properties. Endothelin-1 (ET-1), a potent vasoconstrictor peptide, has been proposed to play a role in the local regulation of aqueous outflow and intraocular pressure (IOP) control. We propose an in vitro culture model as a method for the study of ET-1-induced human TM (HTM) cell contractility and for the study of whether pre-incubation with flunarizine, a calcium-channel blocker, can inhibit the action of ET-1. Experiments were performed on semiconfluent HTM cells (primary cultures established from normotensive human donor eyes) at the second passage, with phosphate-buffered saline (PBS) as a control. The contractile status of the cells was evaluated by a morphometric analysis of cell area, assuming that HTM cells in culture are able to reduce their area as a consequence of cytoskeletal contraction, rather than regulatory volume decrease. After incubation with 10 microM ET-1 for 5 mins, we observed a reduction of HTM cell area with respect to PBS-treated cells: 2425 +/- 876 microm2 versus 3125 +/- 987 microm2 (P < 0.001); and cells exhibited a retraction in shape and a reduction in number of indented profiles. Administration of ET-1 at progressively lower doses produced a corresponding lower reduction of HTM cell area, suggesting a dose-response effect of ET-1. Pre-incubation with 10 microM flunarizine strongly inhibited the ET-1 effect on HTM cell contraction: 2806 +/- 865 microm2 versus 2910 +/- 846 microm2 (P = not significant). Our data indicate that ET-1 induced a statistically significant reduction in the area of HTM cells versus controls, and that ET-1 can directly influence the aqueous outflow. Moreover, we observed that flunarizine inhibited the effect of ET-1 on the HTM cells.

Cells, Cultured↗
PubMed1999

Intracellular Cl regulates Na-K-Cl cotransport activity in human trabecular meshwork cells.

The trabecular meshwork (TM) of the eye plays a central role in modulating intraocular pressure by regulating aqueous humor outflow, although the mechanisms are largely unknown. We and others have shown previously that aqueous humor outflow facility is modulated by conditions that alter TM cell volume. We have also shown that the Na-K-Cl cotransport system is a primary regulator of TM cell volume and that its activity appears to be coordinated with net efflux pathways to maintain steady-state volume. However, the cellular mechanisms that regulate cotransport activity and cell volume in TM cells have yet to be elucidated. The present study was conducted to investigate the hypothesis that intracellular Cl concentration ([Cl]i) acts to regulate TM cell Na-K-Cl cotransport activity, as has been shown previously for some other cell types. We demonstrate here that the human TM cell Na-K-Cl cotransporter is highly sensitive to changes in [Cl]i. Our findings reveal a marked stimulation of Na-K-Cl cotransport activity, assessed as ouabain-insensitive, bumetanide-sensitive K influx, in TM cells following preincubation of cells with Cl-free medium as a means of reducing [Cl]i. In contrast, preincubation of cells with media containing elevated K concentrations as a means of increasing [Cl]i results in inhibition of Na-K-Cl cotransport activity. The effects of reducing [Cl]i, as well as elevating [Cl]i, on Na-K-Cl cotransport activity are concentration dependent. Furthermore, the stimulatory effect of reduced [Cl]i is additive with cell-shrinkage-induced stimulation of the cotransporter. Our studies also show that TM cell Na-K-Cl cotransport activity is altered by a variety of Cl channel modulators, presumably through changes in [Cl]i. These findings support the hypothesis that regulation of Na-K-Cl cotransport activity, and thus cell volume, by [Cl]i may participate in modulating outflow facility across the TM.

Carrier Proteins↗
PubMed1984

Anterior and posterior parts of human trabecular meshwork.

From gonioscopic observations, the trabecular meshwork was tentatively divided into anterior and posterior parts. The anterior part was defined as the zone from the Schwalbe's line to the anterior edge of the Schlemm's canal, and the posterior part was from the anterior edge of the Schlemm's canal to the angle recess. The patients' own blood cells were injected into the anterior chamber of two eyes about to be enucleated due to malignant tumors, and cell distribution in the trabecular meshwork was examined histologically. Blood cells in the posterior part of the trabecular meshwork were numerous, particularly in the area adjacent to the Schlemm's canal and anterior to the ciliary muscle at the angle recess, yet only a few cells were seen in the anterior part. At the angle recess, the blood cells accumulated in the perivascular connective tissue of the major arterial circle of the iris. These observations suggest that the posterior part of the trabecular meshwork is the most important for aqueous humor drainage in the human eye, both with regard to the conventional and unconventional routes, while the anterior part plays a lesser role in the aqueous outflow. It is also suggested that some proportion of the aqueous humor entering the tissues at the angle recess may flow through the perivascular tissue of the major arterial circle of the iris.

Aged↗
PubMed1997

Trabecular meshwork phagocytosis in glaucomatous eyes.

Trabecular meshwork cells are actively phagocytic and may function to keep the drainage pathways free of cellular debris, pigment and other material. A decrease in phagocytic capacity has been proposed in the pathogenesis of glaucoma. This study was performed to compare the phagocytic capability of the human trabecular meshwork in glaucomatous and normal human eyes. The anterior segments of 6 donors with glaucoma (primary open-angle glaucoma, POAG: 5 donors; pseudoexfoliative glaucoma, PEX: 1 donor) and 6 normal donors were placed in perfusion organ culture. During the final 24 h of culture, latex microspheres, labeled with FITC and coated with antibodies, were perfused into the anterior segments. Eyes were then fixed, the trabecular meshworks were treated with a rhodamine-labeled secondary antibody, sectioned and the number of ingested beads determined with the laser scanning confocal microscope. Nuclei were quantitated and used to calculate the phagocytic index of each eye (number of ingested beads/number of nuclei). Anterior segments of glaucomatous donors were cultured for 1-3 days, as a preliminary culture study had revealed that culture of glaucomatous anterior segments is successful in only 50% when cultured for 21 days. Specimens of normal donors were cultured for 21 days. Ingested beads appeared green and could be differentiated from noningested beads, which appeared red, using appropriate wavelengths of the laser. Bead ingestion was confirmed with electron microscopy and the use of a secondary antibody labeled with horseradish peroxidase. Ingestion rates appeared similar among all three groups of eyes: POAG, 3.8 beads/cell; PEX, 3.3 beads/cell; normal, 3.5 beads/ cell. No evidence of significant migration or loss of trabecular cells was noted. Cell counts were not significantly different: POAG, 127 +/- 40 cells/section; normals, 136 +/- 49 cells/section. In conclusion, the phagocytic ability of the trabecular meshwork appears similar between eyes with POAG and normal eyes in perfusion organ culture. Cell loss after phagocytosis was not observed in these single-exposure experiments.

Aged↗
PubMed1979

Glaucoma associated with precipitates on the trabecular meshwork.

Precipitates on the trabecular meshwork may be the only sign of ocular inflammation. Fourteen patients who had glaucoma associated with precipitates on the trabecular meshwork and minimal or no other signs of ocular inflammation did not respond to usual antiglaucoma therapy. Treatment with topical steroids eliminated the precipitates and lowered the intraocular pressure. Careful gonioscopy is the key to accurate diagnosis.

Acetazolamide↗
PubMed1991

[The development of human trabecular meshwork].

The fetal development of the trabecular meshwork of the human eye was quantitatively studied by light and electron microscopy. From the 20th fetal week onward, the progressive thickening of the trabecular meshwork was achieved mainly by the widening of intertrabecular spaces, whereas the thickness and the number of trabeculae were almost constant. Significant alterations in the number of trabecular meshwork cells did not occur with development. However, a decrease in trabecular meshwork cellularity occurred by the widening of intertrabecular spaces. As development proceeded, there was an increase in the proportion of the width of the posterior trabecular meshwork, which is the main site of aqueous drainage, in accordance with the increase of aqueous production.

Cell Count↗
PubMed1994

Lysosomal enzyme and inhibitor levels in the human trabecular meshwork.

PURPOSE: To examine in the human trabecular meshwork lysosomal enzymes and one inhibitor of serine proteases that actively participate in the degradation of macromolecules into low molecular weight constituents. METHODS: Using an avidin-biotin-peroxidase technique, lysosomal proteases and alpha 1-proteinase inhibitor were examined in the trabecular meshwork of 23 human eyes with donor ages ranging from 2 to 90 years. These eyes were categorized into three age groups (< or = 20, 21 to 49, and > or = 50 years). Histochemical staining for lysosomal hydrolases was also performed on frozen sections of 20 human eyes. The staining was analyzed by an image analyzer and the levels of lysosomal proteases were further measured by biochemical assays. RESULTS: The trabecular meshwork from all the eyes stained intensely against antibodies to cathepsins B and G and alpha 1-proteinase inhibitor. The staining for elastase was weaker but evident. Image analyses revealed that the staining intensity for each protease or inhibitor was similar in all age groups. The staining in the uveal meshwork appeared to be the strongest among all the trabecular meshwork regions. Biochemical assays of tissue extracts confirmed that the enzyme and inhibitor levels were comparable among the three donor age groups. Activities of two lysosomal hydrolases, acid phosphatase and acid esterase, were also found in trabecular meshwork cells of 20 eyes. No apparent difference in enzyme activities was found with increasing age, and variation related to region was not observed. CONCLUSIONS: This study demonstrated the age-independent distribution of a variety of lysosomal enzymes and a protease inhibitor in the human trabecular meshwork. The presence of these proteins suggests a possible role in the metabolic operation of the trabecular meshwork.

Adolescent↗
PubMed1988

Human trabecular meshwork organ culture.

Human trabecular meshwork obtained from postmortem eyes was maintained in organ culture condition up to 12 weeks. The explants were dissected into specimens of three different sizes. Types 1 and 2 specimens were larger than 4 mm square and 1 mm thick, and type 3 specimens were about 1 mm3. Each specimen was placed in a depression made in the center of an agar block and the block was placed in a plastic culture dish. The space between the agar block and the culture dish was filled with liquid medium consisting of MEM Eagle supplemented with 10% fetal bovine serum, 10% chick embryo extract and 200 U/ml penicillin G. Afterwards, the explant was incubated in 5% CO2 with 100% humidity. Types 1 and 2 specimens maintained a normal appearance on electron microscopy during the entire 12 weeks of culture, while type 3 specimens showed marked cellular activation and cell loss soon after explantation. Morphometric studies regarding cell number in sections for light microscopy obtained from types 1 and 2 specimens revealed good preservation of trabecular cells during the 12 weeks of culture. Our culture system may be useful in investigating the direct effects produced on human trabecular meshwork by photocoagulation and various agents, for example anti-glaucoma drugs, steroids and viscoelastic materials.

Cadaver↗
PubMedDate not supplied

Regulation of trabecular meshwork contractility.

Ample evidence supports the theory that trabecular meshwork possesses smooth-muscle-like properties. Trabecular meshwork cells express a large number of transporters, channels and receptors, many of which are known to regulate smooth-muscle contractility. It has been shown that trabecular meshwork can be induced to contract and relax in response to pharmacological agents. In the model of the bovine eye, confirmed in some cases by experiments on primates, agents that contract trabecular meshwork reduce outflow. On the cellular level, this is coupled with depolarization and a rise in intracellular calcium. Relaxation of trabecular meshwork, on the other hand, appears to be coupled to a stimulation of the maxi-K channel, inducing hyperpolarization and a closure of L-type calcium channels. No significant differences between cells from a human and a bovine source emerged, either in classical measurements of membrane voltage, in measurements of intracellular calcium or patch-clamp experiments. Thus, pharmacological agents that relax trabecular meshwork seem promising candidates for further research - the ultimate goal being an improvement of glaucoma therapy in humans.

Adrenergic Agonists↗