Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Trabecular Meshwork”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources
PubMed2002

Signaling mechanism of TGF-beta1-induced collagen contraction mediated by bovine trabecular meshwork cells.

PURPOSE: To characterize the intracellular signaling mechanism that underlies the contraction of trabecular meshwork (TM) tissue. METHODS: The contraction of collagen mediated by bovine TM cells was evaluated by measuring changes in the diameter of collagen gels in which the cells were embedded. Changes in the organization of the actin cytoskeleton were examined by laser-scanning confocal microscopy of cells stained with fluorescent phalloidin. Cell motility was monitored by time-lapse video microscopy. RESULTS: Transforming growth factor (TGF)-beta1 induced marked TM-cell-mediated contraction of collagen gels in a concentration- and time-dependent manner. Inhibitors of protein kinase C (PKC) blocked this effect of TGF-beta1, whereas an inhibitor of PKA and -G did not. An inhibitor of the small guanosine triphosphatase (GTPase) Rho also inhibited TGF-beta1-induced collagen contraction, whereas an activator of Rho promoted this effect of TGF-beta1. Furthermore, inhibition either of the release of Ca(2+) from internal stores or of the activation of myosin light-chain kinase (MLCK) prevented gel contraction in response to TGF-beta1. The effects of these various agents on TGF-beta1-induced contraction of collagen gels mediated by TM cells were mirrored by their effects on TGF-beta1-induced formation of actin stress fibers, cell spreading (the extension of cellular processes), and cell motility under conditions in which cell contraction was not possible. CONCLUSIONS: TGF-beta1 induces TM-cell-mediated collagen gel contraction through activation of Rho and the Ca(2+)-dependent enzymes PKC and MLCK. These same signaling molecules contribute to TGF-beta1-induced rearrangement of the actin cytoskeleton, cell spreading, and cell motility.

Actins↗
PubMed2000

Induction of tissue transglutaminase in the trabecular meshwork by TGF-beta1 and TGF-beta2.

PURPOSE: To study whether human trabecular meshwork (HTM) cells are capable of expressing and secreting tissue transglutaminase (tTgase), an enzyme cross-linking extracellular matrix (ECM) proteins, and whether tTgase and synthesis of cross-linked fibronectin are increased after treatment of HTM cells with transforming growth factor (TGF)-beta1 or -beta2. METHODS: Anterior segments of six normal human eyes were stained with antibodies to tTgase. Tissues from three eyes were analyzed for tTgase using Western blot analysis. Monolayer cultures of HTM cells from eyes of five human donors were treated with 1.0 ng/ml TGF-beta1, -beta2, or 5 X 10(-7) M dexamethasone (DEX) for 12 to 96 hours. Induction of tTgase was investigated by Western and Northern blot analysis. External tTgase activity was measured by the ability to form polymerized fibronectin and the incorporation of biotinylated cadaverine into fibronectin. RESULTS: Labeling for tTgase was observed throughout the entire HTM. Cultured HTM cells expressed tTgase intra- and extracellularly. Treatment of cultured HTM cells with TGF-beta1 and -beta2 increased the tTgase mRNA and protein levels, whereas DEX had no effect. TGF-beta-treated HTM cells showed a significant increase in polymerized and unpolymerized fibronectin. Incorporation of biotinylated cadaverine was markedly increased when HTM cells were treated with TGF-beta for 24 hours before seeding. CONCLUSIONS: The enzyme tTgase is expressed in the HTM and is inducible by TGF-beta1 or -beta2 in cultured HTM cells. Extracellular tTgase is able to polymerize fibronectin. Increased levels of TGF-beta2 in the aqueous humor may lead to an increase of tTgase expression and activity in the HTM, causing an increase of irreversibly cross-linked ECM proteins. This mechanism might play a role for the increased outflow resistance seen in glaucomatous eyes.

Adult↗
PubMed1984

Trabecular meshwork cellularity in primary open-angle glaucoma and nonglaucomatous normals.

The trabecular meshwork cellularity (cells/unit tissue area) was compared in patients with primary open-angle glaucoma (POAG) with that of nonglaucomatous (NG) individuals. The NG specimens (n = 69) include specimens from the prenatal period (n = 14) as well as the postnatal period to age 98 years (n = 55). The glaucoma specimens (n = 49) covered a wide-range of ages (23-80 years) and were obtained at trabeculectomy (n = 31) or at autopsy (n = 18). Our results show that the trabecular cellularity in NG specimens decreases most rapidly and in a nonlinear manner in the late fetal period and for the first few years of postnatal life. This rapid decline in cellularity then slows down to proceed in a nearly linear manner for the remainder of the 98 years of life studied. The meshworks from patients with POAG have a lower cellularity than normals over the wide range of ages examined, but both types of specimens undergo similar declines in cellularity with age. Thus, the age-cellularity curves for both the NG and POAG specimens are parallel to each other. The loss of cells occurs in a gradient-like manner with the inner tissues being most affected and the outermost tissues least affected. A variety of statistical tests show that these changes in cellularity are highly significant and specific. These findings are compared to the loss of endothelial cells in the cornea and they are discussed in relation to the important clinical characteristics of POAG.

Adolescent↗
PubMed1995

Migration of cultured bovine trabecular meshwork cells to aqueous humor and constituents.

PURPOSE: To investigate the migration of cultured bovine trabecular meshwork cells to aqueous humor and some of its constituents, and to compare the migration of normally proliferating and growth-arrested cells. METHODS: Cellular migration was evaluated in 48-well microchemoattraction chambers, and the chemoattractants used were bovine aqueous humor, glycoproteins, and growth factors. RESULTS: The meshwork cells responded well to bovine aqueous humor, and antibody neutralization experiments showed that fibronectin accounted for approximately 40% of aqueous chemoattraction. The glycoproteins laminin, thrombospondin, and transferrin elicited only modest migratory activity. Platelet-derived growth factor was the most powerful chemoattractant of the growth factors tested, and the others produced moderate migratory effects. Basic fibroblast growth factor was not chemoattractive on its own but stimulated migration when combined with heparin. Growth-arrested cells showed less migration to a standardized chemoattractive stimulus than did proliferating meshwork cells. CONCLUSIONS: For the first time, aqueous humor was shown to act as a migratory stimulus for meshwork cells in vitro. The major attractant is fibronectin; the remaining active constituents must still be identified.

Animals↗
PubMed1987

Effect of vitamin A on glycoconjugate: synthesis in the trabecular meshwork. A preliminary report.

We studied the effect of vitamin A on glycoconjugate synthesis in trabecular meshwork (TM) cells in vivo. The aqueous flow system of two cats and one monkey was exposed in vivo to retinoic acid dissolved in dimethyl sulfoxide (DMSO). One hour prior to enucleation, [3H]glucosamine was injected into all eyes. The tissue was subsequently processed for autoradiography. The density of grains (grains micron-2) in the vitamin A-treated eyes of Cats I and II was 77% and 30% less, respectively, than the density of grains in the control eyes. In the monkey the grain density was 56% less in the experimental eye compared with the control eye. These data suggest that exogenous vitamin A suppresses glycoconjugate synthesis in TM cells in vivo.

Animals↗
PubMedDate not supplied

Aging of trabecular meshwork cells of the human eye in vitro.

A monolayer cell line established from the trabecular meshwork of a human eye exhibited a limited proliferation potential with about 18 population doublings (PD). There was a gradual increase of the average PD time with increasing PD level. Finally, there was complete growth cessation. These non-replicating cells were larger and more flattened (decrease of the saturation density); they became granulated and finally died off in the course of several months. This growth pattern resembled the senescence phenomenon, as originally described by Hayflick and Moorhead for cultured human fibroblasts. In comparison to proliferating phase-II cultures, senescent cultures revealed reduced glycosaminoglycan synthesis rates with a relative decrease of hyaluronic acid and increase of heparan sulfate. Exogenous (medium-supplied) hyaluronic acid or ascorbic acid stimulated hyaluronic acid synthesis of phase-II cultures.

Ascorbic Acid↗
PubMed1995

[The effect of steroids on organ-cultured porcine trabecular meshwork--an ultrastructural, biochemical, and lectin histochemical study].

The effect of corticosteroid administration on porcine trabecular meshwork (PTM) was studied by ultrastructural and biochemical analysis. Electron microscopic observations showed an increase of elastic fibers in PTM treated with steroids. Two-dimensional polyacrylamide gel electrophoresis with silver staining showed an increase of proteins with molecular weights of 52 kDa, 66 kDa and 70 kDa. The 66 kDa protein was assumed to be a glycoprotein containing N-acetyl-D-glucosamine, as it was stained positively in the lectin blot analysis with Triticum vulgaris (WGA) and Datura stramonium (DSA). The elastic fibers reacted positively to WGA and DSA, and the degree of this reaction was strengthened by steroid treatment. These results demonstrated that steroid treatment induces ultrastructural and biochemical changes in PTM, and an increase of elastic fibers containing glycoprotein with N-acetyl-D-glucosamine.

Acetylglucosamine↗
PubMed1994

Localisation of alpha(2,3) and alpha(2,6) linked terminal sialic acid groups in human trabecular meshwork.

Sialic acid specific lectins were used to localise isomers of sialyl glycosides in human trabecular meshwork (TM) at the ultrastructural level. A lectin immunogold method demonstrated that sialic groups were concentrated on the endothelial surface of Schlemm's canal (SC) and in the adjacent juxta-canalicular tissue (JCT). One sialyl glycoside, alpha(2,6) linked N-acetyl neuraminic acid, was present mainly on the luminal aspect of the SC endothelium and in the cytoplasm of the JCT cells. Another, alpha(2,3) linked N-acetyl neuraminic acid, was localised predominantly to the extracellular fibrillar material of the JCT. The existence of a topographical segregation of these two sialyl glycosides within the TM supports the view that highly charged anionic molecules may be of significance in regulating aqueous outflow.

Adult↗
PubMed2004

Immunolocalization of prostanoid EP receptor isotypes in human trabecular meshwork.

PURPOSE: To assess the localization of the EP-type prostanoid receptors in the human trabecular meshwork (TM) and to determine their spatial distribution in relation to the contractile a-smooth muscle actin fibres. METHODS: Cryosections of human anterior segments were obtained from 17 different donors and immunostained with different EP receptor subtype specific antibodies. Double staining for the EP2 receptor and smooth muscle actin was carried out. Western blots of TM protein samples were studied. RESULTS: No specific staining for the EP1 receptor was observed. The antibodies against the EP2 receptor revealed in all donors intense staining of human trabecular cells throughout the meshwork. EP3 receptor specific staining was not detected. EP4 immunostaining was confined to the corneoscleral region near Schwalbe's line. On western blots, the EP2 receptor was detected. In the posterior TM, the EP2 receptor staining was associated with the dense network of actin fibres. CONCLUSIONS: These immunocytochemical results present evidence that the EP2 receptor is the most abundantly expressed isotype of the PGE receptors in the human TM. This conclusion is in agreement with our previous findings at the transcript level. The relaxant responses of the TM to application of EP2 receptor agonists, and flow enhancement evoked by prostaglandin PGE1, may be explained by the close spatial association of the EP2 receptor with actin fibres.

Actins↗
PubMed1999

How does the trabecular meshwork regulate outflow? Clues from the vascular endothelium.

Although it is well known that the trabecular meshwork plays a central role in regulating the outflow of aqueous humor from the eye, the cellular mechanisms and events responsible for this function are poorly understood. In contrast, the mechanisms by which vascular endothelial cells modulate the permeability of blood vessels have been more thoroughly investigated. It is hypothesized that the cells of the TM employ mechanisms similar to those observed in the vascular endothelium to modulate aqueous humor permeability. Specifically, it is hypothesized that the cells of the TM employ Na-K-Cl cotransport to modulate their intracellular volume and thus the volume of the paracellular pathways through which aqueous humor may travel. The current knowledge about the role of Na-K-Cl cotransport and volume regulation in the regulation of vascular permeability, and evidence that similar physiologic events occur in the TM are reviewed. In addition, the implications for further study of aqueous humor outflow physiology are discussed.

Aqueous Humor↗
PubMed2004

[The effect of growth factors on the proliferation of cultured porcine trabecular meshwork cells].

PURPOSE: We attempted to identify cell growth factors that cause a multiplication of trabecular meshwork(TM) cells. METHODS: Porcine TM cells were cultured in Dulbecco's modified Eagle's medium/nutrient mixture F-12/Ham to which we added 1, 10, and 100 ng/ml of platelet-derived growth factor(PDGF), fibroblast growth factor 2(FGF2), insulin-like growth factor-1 (IGF-1), vascular endothelial cell growth factor(VEGF), hepatocyte growth factor (HGF), or brain-derived neurotrophic factor(BDNF). We measured [3H] thymidine incorporation to evaluate the influence of the growth factors on TM cell proliferation. RESULTS: [3H] thymidine incorporation into TM cells was promoted by 10 and 100 ng/ml of PDGF, IGF-1, and FGF2 after 24 and 48 hours, whereas 1, 10, and 100 ng/ml of VEGF restrained cell proliferation after 48 hours. HGF and BDNF did not show any remarkable influence on TM cell proliferation. CONCLUSIONS: Our, results suggest that PDGF, IGF-1, and FGF2 may cause a drop in intraocular pressure followed by activation of a TM function, by multiplying TM cells.

Animals↗
PubMedDate not supplied

Transmission electron microscopic analysis of trabecular meshwork in secondary glaucoma after intravitreal silicone oil injection.

PURPOSE: We analyzed morphological changes in trabecular meshwork in glaucoma developing after intravitreal silicone oil injection with transmission electron microscopy (TEM). METHODS: Specimens obtained from 2 patients after surgical trabeculectomy were fixed in McDowell fixative in one patient and in buffered formaldehyde in the other, dehydrated and embedded in Epon. Ultrathin sections were made and stained with lead citrate and uranyl acetate for TEM. RESULTS: In specimens mainly connective tissue sheets with disorganized and narrowed intertrabecular spaces were observed. At higher magnification the collagen sheets were composed of interstitial collagen and some of them were covered by amorphous basal membrane structures resembling material. Cellular remnants were present along the intertrabecular spaces. No other cells or clearly evident silicone oil were noted. CONCLUSION: Changes such as decrease in cell content, fibrosis and build-up of basement membrane-like material have been described by other authors. They are not specific and can be seen in many secondary glaucomas. No macrophages and foreign-body granulomas in response to silicone oil were present. The pathological changes in angle structures are probably caused by other mechanisms and are not induced by silicone oil itself.

Collagen↗
PubMed2002

Adenylyl cyclase activity mediated by beta-adrenoceptors in immortalized human trabecular meshwork and non-pigmented ciliary epithelial cells.

Non-pigmented ciliary epithelial (NPE) and trabecular meshwork (TM) cells are important in maintaining normal aqueous humor dynamics through the inflow and outflow routes, respectively. The current studies were undertaken to evaluate the ability of several beta-adrenergic receptor agonists to stimulate various antagonists to inhibit cAMP production in cultured immortalized human TM and NPE cells using an automated enzyme immunoassay. Isoproterenol was the most potent agonist in both the NPE and TM cells. The rank order of potency of agonists in NPE and TM cells, respectively, was: isoproterenol [EC50 = 37 and 66 nM] > epinephrine [EC50 = 112 and 526 nM] > albuterol [EC50 = 426 and 785 nM] > norepinephrine [EC50 = 3 and > 10 microM] > phenylephrine [EC50 > 10 microM for both] = dopamine [EC50 > 10 microM for both](n = 3-19). The isoproterenol-induced cAMP production was inhibited by various antagonists with the following rank order of potency in NPE and TM cells, respectively: propranolol [Ki = 0.2 and 0.3 nM] = ICI-118551 [Ki = 0.5 and 0.4 nM] > levobunolol [Ki = 1.1 and 2.1 nM] > levobetaxolol [Ki = 13 and 14 nM] = racemic betaxolol [Ki = 43 and 19 nM] > dextrobetaxolol [Ki = 2,705 and 1,980 nM] > atenolol [Ki > 4,000 nM for both] (n = 3-7). These detailed pharmacological studies using a variety of agonists and antagonists further supported the presence of beta2-adrenergic receptors in immortalized human NPE and TM cells.

Adenylyl Cyclases↗
PubMed1998

[An experimental study on mechanism of intraocular pressure decline after allogeneic transplantation of trabecular meshwork].

OBJECTIVE: To study the mechanism of intraocular pressure (IOP) decline after allogeneic transplantation of trabecular meshwork (TM) in primate experimental glaucoma. METHODS: The experimental open-angle glaucoma models were created in 8 rhesus monkey eyes by repeated pangoniophotocoagulation on functional TM using argon laser. After 2, 3, 5 months respectively, avidin-gold or self-erythrocytes, which acted as tracers of the aqueous humor outflow, were perfused into the anterior chamber under normal pressure and volume conditions. 30 minutes later, 2.5% glutaraldehyde was perfused into the anterior chamber under the same conditions. Allograft TMs and photocoagulated area (serving as the control) were observed by light, transmission, scanning electron microscopy and ultrahistochemistry study. RESULTS: The IOP of 5 eyes of 6 experimental eyes became normal. A blood reflux into Schlemm's canal was seen by gonioscopy in 4 eyes. The surface of TMs from graft showed the normal uveal TM cords and intertrabecular spaces. Erythrocytes were found in the intertrabecular spaces and Schlemm's canal. Avidin-gold and vacuolar containing gold were observed in the cells of TM and Schlemm's canal. The TMs of photocoagulated area appeared to be fewer and narrower intertrabecular spaces. The uveal cords of this zone were confused. The content of acid mucopolysaccharides in the grafts was closer to normal than that in the photocoagulated areas. CONCLUSION: TM of allogeneic transplantation not only can survive but also function as an aqueous humor outflow pathway. We consider that this operative procedure can be used for treatment of some cases with glaucoma cautiously.

Animals↗
PubMed1996

Pharmacological characterization of bradykinin receptors coupled to phosphoinositide turnover in SV40-immortalized human trabecular meshwork cells.

This study sought to pharmacologically characterize bradykinin receptors on SV40-immortalized human trabecular meshwork (HTM3) cells. Phosphoinositide (PI) turnover studies were conducted using [3H]myo-inositol-labeled HTM3 cells and anion exchange chromatography to quantify [3H]inositol phosphates generated in response to bradykinin (BK) and various BK analogs. The blockade of these responses was studied using two potent and receptor-subtype selective antagonists. BK and T-kinin (Ile-Ser-BK:TK) induced a 4.2-4.4 fold stimulation of PI turnover above base levels at 1-10 microM. Several other peptides unrelated to BK, including angiotensin II, endothelin, cholecystokinin, bombesin and peptide YY tested at 1-10 microM were essentially inactive. The molar potencies (EC50) of BK, TK and close analogs were: BK = 4.5 +/- 0.5 nM (n = 6), Lys-BK = 6.5 +/- 0.7 nM (n = 3), TK = 38.8 +/- 6.6 nM (n = 8), Met-Lys-BK = 41.5 +/- 13.4 nM (n = 4), Des-Arg9-BK = 2093 +/- 626 nM (n = 4). All the latter BK-related peptides were full agonists. The actions of BK and TK were potently and competitively antagonized by Hoe-140 (molar potency = 0.6-1 nM; pA2 = 8.97-9.21. n = 3-4) and by D-Arg0[Hyp3,-Thi5.8,-DPhe7]-BK (molar potency = 251 nM; -log potency, pKb = 6.6), two selective B2-type BK antagonists. In conclusion, rank order of potency of BK agonists and the blockade of BK- and TK-induced PI turnover by the selective antagonists are consistent with the classification of the BK receptors on HTM3 cells as the B2-receptor subtype.

Aged↗
PubMed2003

Gene expression profile of the human trabecular meshwork: NEIBank sequence tag analysis.

PURPOSE: To characterize the gene expression pattern in the human trabecular meshwork (TM) and identify candidate genes for glaucoma by expressed sequence tag (EST) analysis as part of the NEIBank project. METHODS: RNA was extracted from dissected human TM and used to construct unamplified, un-normalized cDNA libraries in the pSPORT1 vector. More than 4000 clones were sequenced from the 5' end. Clones were clustered and identified using GRIST software. In addition, the expression patterns of genes encoding olfactomedin-domain proteins were analyzed by RT-PCR. RESULTS: After non-mRNA contaminants were removed, 3459 independent TM-expressed clones were obtained. These were grouped in 1888 clusters, potentially representing individual expressed genes. Transcripts for the myocilin gene, a locus for inherited glaucoma, formed the third most abundant cluster in the TM collection, and several other genes implicated in glaucoma (PITX2, CYP1B1, and optineurin) were also represented. One abundant TM transcript was from the gene for the angiopoietin-like factor CTD6, which is located at on the long arm of chromosome 1, area 36.2-36.1 in the region of the glaucoma locus GLC3B, whereas other transcripts were from genes close to known glaucoma loci. The TM collection contains cDNAs for genes that are preferentially expressed in the lymphatic endothelium (matrix Gla protein, apolipoprotein D precursor, and selenoprotein P precursor). In addition to EST profiling, RT- PCR was used to detect transcripts of the olfactomedin-domain proteins latrotoxin receptor Lec3 and optimedin in the TM. CONCLUSIONS: The TM libraries are a good source of molecular markers for TM and candidate genes for glaucoma. The abundance of myocilin cDNAs corresponds to the critical role of this gene in glaucoma and contrasts with libraries derived from cultured tissue. The expression profile raises the possibility that cells of the TM and Schlemm's canal may be more similar to lymphatic, rather than blood vascular endothelium.

Aged↗
PubMed1997

Effects of dexamethasone on sodium-potassium-chloride cotransport in trabecular meshwork cells.

PURPOSE: Previous studies in the authors' laboratory have shown that bovine and human trabecular meshwork (TM) cells possess a robust sodium-potassium-chloride (Na-K-Cl) cotransport system that functions in regulating intracellular volume and may play a central role in modulating outflow facility across the TM. Dexamethasone, which can induce ocular hypertension, has been found to increase resistance to aqueous outflow across the TM. The current study was conducted to investigate the hypothesis that alteration of TM cell Na-K-Cl cotransport function, regulation, or both may be an underlying factor in steroid-induced glaucoma. To this end, the authors evaluated the effects of dexamethasone treatment of TM cells on Na-K-Cl cotransport activity and cotransporter protein expression. METHODS: Cultured bovine and human TM cell monolayers were exposed to dexamethasone (10(-9) to 10(-6) M) for varying times, then evaluated for Na-K-Cl cotransport activity or harvested for cellular membrane proteins. Cotransport activity was assessed as bumetanide-sensitive K influx. Cotransport protein expression was evaluated by Western blot analysis of cellular proteins using a monoclonal antibody to the human colonic T84 epithelial cell Na-K-Cl cotransporter. RESULTS: The authors found that 24- and 48-hour exposures of human and bovine TM cells to dexamethasone stimulates Na-K-Cl cotransport activity (10(-8) to 10(-6) M dexamethasone in human cells; 10(-8) and 10(-7) M in bovine cells). The authors also found that dexamethasone (10(-8) M) stimulates Na-K-Cl cotransport activity of TM cells with exposure times as early as 12 hours and up to 5 days. In addition, the authors found that the level of Na-K-Cl cotransport protein expressed in TM cells is modulated by dexamethasone. When bovine or human TM cells are exposed to 10(-8) or 10(-6) M dexamethasone for 2 to 5 days, cotransporter protein expression is increased. With longer exposures, however, cotransporter protein levels decrease below control levels. Finally, the authors found that TM cells exposed to dexamethasone become unresponsive to regulation by hypertonicity and vasopressin. CONCLUSIONS: The authors' findings suggest that dexamethasone may be exerting its effect, at least in part, through altering Na-K-Cl cotransport function and regulation in TM cells.

Animals↗
PubMed1994

[Dexamethasone effects of protein synthesis on organ-cultured human trabecular meshwork--autoradiographical, biochemical, and immunohistochemical study].

The effect of dexamethasone (DEX) on organ-cultured human trabecular meshwork (HTM) was evaluated autoradiographically, biochemically, and immunohistochemically. The tissues were obtained from 11 normal postmortem individual eyes, aged 15-84 years. In 2 individuals, 2-week treatment of cultured HTM with DEX (1 x 10(-4) M, 1 x 10(-5) M, 1 x 10(-6) M) induced the expression of 35S-methionine-labelled cell proteins of 40, 55, and 66 kD which were not present in HTM cultures with out DEX treatment. In electron microscopic autoradiography of the same cases, trabecular cells containing numerous intracytoplasmic vacuoles were seen and silver grains were found on microfibrils in the intracytoplasmic vacuoles. In addition, in immunoblot analysis of anti-alpha elastin of the same cases, a 72 kD band representing elastin was seen and DEX treatment showed stronger reactivity than the control. In immuno-electron microscopy of the same cases, elastin was localized on the surface of trabecular cells containing numerous intracytoplasmic vacuoles. In the remaining 9 individuals, there were no significant differences between control and DEX treatment. The alterations in the proteins/glycoproteins and elastin produced by DEX observed in organ-cultured HTM may play a role in the reduction in aqueous outflow facility observed clinically in steroid glaucoma.

Aged↗