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PubMed1998

Investigation of the 'fines' hypothesis of primary open-angle glaucoma: the possible role of alpha-crystallin.

Primary open-angle glaucoma is a disease caused by an increase in intraocular pressure due to a decreased facility of outflow of aqueous humor through the trabecular meshwork. The etiology of primary open-angle glaucoma is currently unknown, but it has been suggested that one possible mechanism may be the obstruction of flow through the trabecular meshwork by small macromolecules, analogous to the effect of 'fines' in column chromatography. One such candidate is alpha-crystallin, a lens protein which may be released into the aqueous humor from lens fiber cells at concentrations below that necessary for the formation of the native aggregate. Results of in vitro binding experiments indicate that alpha-crystallin and serum albumin, which is secreted at the anterior root of the iris and is believed to act as a protein escort through the trabecular meshwork in mammalian eyes, will interact at concentrations of alpha-crystallin up to the critical micelle concentration for alpha-crystallin (3.5-5 mg/ml, or 0.18-0.25 mM). There is little interaction at or above this concentration. This binding could serve the necessary function of preventing interactions between alpha-crystallin monomers or small aggregates and hydrophobic surfaces within the trabecular meshwork. Since, however, the interaction between the two proteins is not extremely strong, the accumulation of unbound alpha-crystallin monomers and/or dimers could contribute to the development of primary open-angle glaucoma.

Animals↗
PubMed1977

The outflow tract in pigmentary glaucoma: a light and electron microscopic study.

Buttons obtained by trephination from both eyes of a 44-year-old myopic man with pigmentary glaucoma were studied by light and electron microscopy. Although clinically both eyes exhibited heavy pigmentation of the trabecular meshwork in the whole circumference, microscopically the trabecular meshwork of the left eye contained more pigment granules than that of the right eye, which appeared relatively acellular with collapse of the trabecular sheets. In both eyes endothelial cells covering the trabecular sheets were filled with pigment and showed various stages of degeneration. The intertrabecular spaces contained free pigment granules as well as cell debris. These observations suggest that plugging of the trabecular spaces by pigment and cell debris together with fragmentation and collapse of trabecular sheets contribute to the decrease in the facility of outflow that occurs in pigmentary glaucoma.

Endothelium↗
PubMed1997

Anterior segment physiology after bumetanide inhibition of Na-K-Cl cotransport.

PURPOSE: To determine the effect of bumetanide inhibition of Na-K-Cl cotransport on aqueous humor formation and outflow facility in living cynomolgus monkeys, outflow facility in organ-cultured human eyes, and contraction in bovine ciliary muscle and trabecular meshwork strips, in vitro. METHODS: Aqueous humor formation in monkeys was measured fluorophotometrically for 6 hours, 1 to 6 weeks before, immediately after, and 2 to 6 weeks after bumetanide was administered intravitreally (final concentration approximately 100 or 500 microM) or intravenously (0.01 or 0.03 mg/ kg at 0 and 3 hours). Outflow facility in monkeys was determined by two-level, constant-pressure perfusion of the anterior chamber for 45 to 60 minutes before and after bumetanide was administered by bolus intracameral injection (100 microM, initial anterior chamber concentration) or by exchanging the anterior chamber with 2 ml 10, 100, or 500 microM bumetanide. Urine volume was measured 3 hours after administration of intravenous bumetanide in various diluents. The effect on intraocular pressure in organ-cultured human eyes was determined for 48 hours by constant-flow-variable-pressure perfusion with 10 microM bumetanide. Contraction of fresh bovine ciliary muscle and trabecular meshwork was measured isometrically with a force-length transducer system after exposure to 100 microM bumetanide +/-1 microM carbachol. RESULTS: The bumetanide concentrations used had little effect on outflow facility or on aqueous humor formation in normal monkeys, on intraocular pressure in organ-cultured human eyes, or on contraction of bovine ciliary muscle and trabecular meshwork strips. Intravenous bumetanide increased urine volume, regardless of the diluent used. CONCLUSIONS: These results suggest that Na-K-Cl cotransport is not involved functionally in regulation of aqueous humor inflow and outflow and in contractility of ciliary muscle and trabecular meshwork.

Aged↗
PubMed2000

Low doses of pilocarpine do not significantly increase outflow facility in the cynomolgus monkey.

Low doses (10(-9)-10(-6) M) of pilocarpine reportedly increase outflow facility in the organ-cultured human eye, suggesting a direct action on the trabecular meshwork. M3 muscarinic receptors have been found in both cultured human trabecular meshwork cells and tissue. We determined whether low pilo doses would increase outflow facility in the living monkey. The anterior chambers of both eyes of 17 pentobarbital anesthetized cynomolgus monkeys were cannulated and outflow facility measured bilaterally by 2-level constant pressure perfusion after an initial 2 ml exchange with Bárány's perfusand containing 24.5 microM phenylephrine (PE). Two subsequent exchanges were performed with one eye receiving Bárány's + PE + 10(-10)-10(-4) M pilocarpine and the contralateral eye receiving only Bárány's + PE. Outflow facility was measured for 35-40 min following each exchange. Accommodation and pupil diameter were measured before each exchange and approximately every 10 min during facility measurements. Outflow facility was significantly increased by 154 and 313% in eyes treated with 10(-5) M and 10(-4) M pilocarpine, respectively, related to contralateral controls. Accommodation and miosis also were induced only at 10(-5) M (accommodation, 3.3 +/- 1.6 diopters, NS; miosis, -4.1 +/- 0.5 mm, P < or = 0.001) and 10(-4) M (accommodation, 10.6 +/- 0.0 diopters, P < or = 0.02; miosis, -3.4 +/- 1.0 mm, P < or = 0.025) pilocarpine. We conclude that low anterior chamber doses of pilocarpine do not increase outflow facility in the living monkey as reported in the organ-cultured human eye, nor do they induce miosis or accommodation. All three parameters respond to pilocarpine at similar doses, and there is no functional evidence of a meaningful outflow facility-relevant pilocarpine effect on the trabecular meshwork at doses lower than those which affect the ciliary muscle.

Accommodation, Ocular↗
PubMed1985

[Surgical indications in glaucoma].

A number of aspects of glaucoma surgery are discussed. Complete drainage of the aqueous via the subconjunctival space results in underperfusion of the trabecular meshwork, leading to significant impairment of the trabecular function. In certain cases, therefore, we prefer trabeculotomy, even though its pressure-lowering effect is inferior to that of fistulizing surgery: trabeculotomy preserves the unaffected trabecular meshwork. Laser trabeculoplasty has the advantage of increasing the outflow facility. In angle-closure glaucoma, iridectomy is performed as an initial procedure in every case in order to eliminate pupillary block. The transcorneal approach ensures watertight wound closure and preserves the conjunctiva for fistulizing surgery if necessary. Glaucoma surgery can usually be performed in lid akinesia and subconjunctival infiltration. This alternative helps to avoid retrobulbar injection when the optic nerve is already severely damaged by glaucoma.

Anesthesia, Local↗
PubMed2004

Trabecular bypass stents decrease intraocular pressure in cultured human anterior segments.

PURPOSE: To determine the effect on intraocular pressure (IOP) of bypassing the trabecular meshwork in cultured human anterior segments. DESIGN: Prospective laboratory investigation using normal human eyes obtained at autopsy. METHODS: Anterior segments from 21 eyes were placed in perfusion culture, and trabecular bypass stents were inserted through the trabecular meshwork, with the lumen of the tube opening into Schlemm's canal. Eyes received from one to four stents, placed equidistant apart. In eyes receiving one or two stents, additional stents were later added to a maximum of four per eye. RESULTS: Intraocular pressure was lowered after placement of a single stent, from 21.4 +/- 3.8 mm Hg to 12.4 +/- 4.2 (P < .001). This corresponded to an 84% increase in facility of outflow. Eyes receiving more than one stent had final IOP of 11.9 +/- 3.7 mm Hg. Nine eyes had sequential addition of stents, and seven of these had a further decrease of IOP (13.6 +/- 4.1 to 10.0 +/- 4.3; P = .02). Excision of the entire meshwork, between stents, dropped IOP to 6.3 +/- 3.2 mm Hg, indicating some residual meshwork or canal resistance remained even after placement of three stents. CONCLUSIONS: Bypass of the trabecular meshwork lowers IOP in cultured human anterior segments. One stent produced the greatest change in pressure. The sequential addition of more stents further lowered pressure in seven of nine eyes. This technique holds promise as a new clinical surgery for glaucoma.

Anterior Eye Segment↗
PubMed2000

Identification and expression of a novel type I procollagen C-proteinase enhancer protein gene from the glaucoma candidate region on 3q21-q24.

A novel human Type I procollagen C-proteinase enhancer protein-like gene, PCOLCE2, was identified by sequencing an EST in the primary open-angle glaucoma (POAG) region on 3q21. The total cDNA encoded a 415-amino-acid protein that has 43% identity to the Type I procollagen C-proteinase enhancer protein (PCOLCE1). PCOLCE2 contains two CUB domains, which are thought to be involved in protein-protein interactions, and an NTR module. PCOLCE2 message is expressed in the trabecular meshwork, lungs, heart, brain, liver, skeletal muscle, kidney, pancreas, and placenta as a 2-kb message. PCOLCE2, a 52-kDa protein, is expressed in the trabecular meshwork. A novel gene, PCOLCE2, has been identified and characterized. Based upon its homology with collagen-binding proteins, its expression in the trabecular meshwork, and its chromosome location, PCOLCE2 is a candidate gene for GLC1C. However, no coding sequence mutations were detected in PCOLCE2 in a POAG patient from the GLC1C family.

Animals↗
PubMed1989

Ultrastructural changes in the aqueous outflow apparatus of beagles with inherited glaucoma.

Spontaneous glaucoma in the beagle was exhibited after 6 months of age by elevated intraocular pressures and open iridocorneal angles followed by secondary changes. In order to appreciate alterations of the aqueous outflow apparatus in dogs with this autosomal recessive disorder, the eyes of beagles with inherited glaucoma at ages 1 day through 34 months were examined by light, scanning and transmission electron microscopy. Developmentally, no notable differences were observed between normal and preglaucomatous outflow channels through 7 months of age. In 12-month-old glaucomatous chamber angles clustered basement membrane-like material was found scattered throughout the outer corneoscleral trabecular meshwork. In this region elastin-like fibers appeared to be more numerous and arranged less regularly than age-matched normal eyes. Occasional trabecular cells within the corneoscleral trabecular meshwork possessed small clusters of serrated, opaque rods within their cytoplasm. In the older glaucomatous dogs these changes were more generalized and extensive throughout the entire corneoscleral trabecular meshwork. In some individual eyes the anterior chamber angles were observed to be narrow both clinically and histologically. These outflow apparatuses were additionally characterized by compressed, less organized trabeculae with a concomitant build-up of extracellular materials. No correlation was found between the shallowness of the iridocorneal angle and increase in intraocular pressure. Primary glaucoma in the beagle during its earlier phases compared more positively to open-angle glaucoma in man than any of the other spontaneous types in animals.

Animals↗
PubMed2005

Immunolocalization of CYP1B1 in normal, human, fetal and adult eyes.

CYP1B1 is a cytochrome P450 enzyme implicated in autosomal recessive primary congenital glaucoma (PCG). The mechanism and function of CYP1B1 in the development of the PCG phenotype is unknown. Previously, investigators have reported detection of Cyp1b1 mRNA in the ciliary body and epithelium and neuroepithelium in the developing mouse eye, employing in situ hybridization techniques. Similarly, additional investigators have detected CYP1B1 mRNA in the iris, ciliary body, non-pigmented ciliary epithelial line, cornea, retinal-pigment epithelium, and retina in the human adult eye, using Northern blotting. This study was designed to immunolocalize CYP1B1 protein in the various ocular structures of normal, human fetal and adult eyes. Normal fetal and adult eyes were immunolabeled with a polyclonal antibody against human CYP1B1 using indirect immunofluorescence, and then compared with appropriate controls. The intensity of immunolabeling of the various ocular structures was assessed by qualitative and semi-quantitative techniques. In the anterior segment anti-CYP1B1 immunoreactivity (IR) was detected early in fetal development in the primitive ciliary epithelium. As well, the most intense CYP1B1 IR was in the non-pigmented ciliary epithelium. In addition, CYP1B1 IR was also present in the corneal epithelium and keratocytes, both layers of the iris pigmented epithelium, and retina. However, CYP1B1 IR was absent in the trabecular meshwork in all of the samples. In general, CYP1B1 immunolabeling in the human fetal eyes was more intense when compared to adult eyes. CYP1B1 IR was primarily immunolocalized to the non-pigmented ciliary epithelium and early in fetal development. In addition, CYP1B1 IR was not detected in the trabecular meshwork. These findings suggest that the abnormalities in the development of the trabecular meshwork in PCG may result from diminished or absent metabolism of important endogenous substrates in the ciliary epithelium due to non-functional CYP1B1 enzyme.

Adult↗
PubMed2000

Synthesis pattern of matrix metalloproteinases (MMPs) and inhibitors (TIMPs) in human explant organ cultures after treatment with latanoprost and dexamethasone.

PURPOSE: To determine changes in production of matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMPs) in the ciliary body, the trabecular meshwork and the retinal pigment epithelium induced by both prostaglandins and corticosteroids. METHODS: Explant organ cultures were removed by a scleral incision 3 mm posterior to the limbus. Retinal pigment epithelium was grown to confluence. Organ and cell cultures were treated with latanoprost and/or dexamethasone for 72 h. The activity of MMP-2, -3 and -9 was assessed using zymography. The synthesis pattern of MMPs and TIMP-1 and -2 was identified using immunostaining. RESULTS: Treatment of explant organ cultures with 10 micrograms/ml of latanoprost induced a mean upregulation of MMP-2 by 36%, MMP-3 by 112% and MMP-9 by 156% as seen by zymography. Dexamethasone 500 nm reduced the amounts of secreted MMP-2 by 13%, MMP-3 by 69%. MMP-9 was not detectable in the media of corticosteroid-treated explant organ cultures. The addition of 10 micrograms/ml of latanoprost to dexamethasone-treated cultures increased MMP-2 by 14%, MMP-3 by 43% and MMP-9 by 49%. Using immunohistochemistry we found staining with antibodies against MMP-2, -3, -9 and TIMP-1 and -2 within the ciliary body, and only to a lesser degree in the trabecular meshwork. Latanoprost treatment caused an increase of 29% in MMP-2 (p < 0.0001), 98% in MMP-3 (p < 0.0001) and 108% in MMP-9 (p < 0.0001). Dexamethasone reduced the staining for MMP-2 by 32% (p < 0.0001), for MMP-3 by 33% (p < 0.0001) and for MMP-9 by 83% (p < 0.0001). Almost no change in staining for MMPs was detectable in the trabecular meshwork. Neither latanoprost treatment nor dexamethasone induced significant changes (p < 0.93) in the secretion of TIMPs. In the media of non-treated retinal pigment epithelium (RPE) cells the only MMP detected was MMP-2. RPE cells in culture did not respond to either treatment with a change in their MMP secretion. CONCLUSION: We detected a profound upregulation of both MMP-3 and MMP-9 and a mild induction of MMP-2 through latanoprost in the ciliary body, but not the trabecular meshwork or RPE cells. Corticosteroids, on the other hand, downregulated MMP expression in both tissues. This inhibiting effect of corticosteroids on MMP production was reversed by latanoprost.

Aged↗
PubMed1990

Stimulation of cell division by argon and Nd:YAG laser trabeculoplasty in cynomolgus monkeys.

Although laser treatment of the trabecular meshwork is the most common form of surgery for glaucoma, the tissue response to this therapy is still incompletely understood. We applied argon or Nd:YAG laser to the trabecular meshwork of six monkeys. Cell division was identified by injecting tritiated thymidine into the anterior chamber 24 hr after laser application. Autoradiography of tissue sections revealed significantly more labelled cells in eyes treated with laser than in the untreated controls. In addition, cells in neighboring tissues such as iris, ciliary body and sclera showed labelling in association with laser application. Furthermore, comparison of argon-induced lesions with those caused by pulsed Nd:YAG suggests that there are quantitative and qualitative differences in the response of trabecular meshwork and surrounding tissues to these two forms of laser energy.

Animals↗
PubMed2000

Absence of trabecular meshwork-inducible stretch response (TISR)/oculomedin gene and proximal promoter mutation in primary open angle glaucoma patients.

We investigated the coding exon and promoter sequence in the trabecular meshwork-inducible stretch response (TISR)/oculomedin gene for mutations in Chinese primary open angle glaucoma (POAG) subjects. The entire TISR/oculomedin coding sequence, together with 138 bp of promoter sequence 5' to the start codon and 170 bp of the 3' untranslated region in 110 Chinese POAG patients and 108 unrelated control subjects without glaucoma, aged 50 years or above, were screened for alterations by DNA sequencing. One heterozygous sequence alteration, K28E, was identified in one control subject, and two homozygous sequence alterations, K28K and 135+36delC, were universally found in every sample. As a result, no common TISR/ oculomedin coding sequence nor any proximal promoter mutation that causes POAG was found. The effect of TISR/ oculomedin in glaucoma has yet to be established.

Adolescent↗
PubMed1995

Identification of an extensive system of nitric oxide-producing cells in the ciliary muscle and outflow pathway of the human eye.

PURPOSE: Nitric oxide (NO) is an important intracellular and intercellular regulator in nerve tissue as well as in vascular endothelium, smooth muscle, and certain other cell types. In the ocular anterior segment, studies in rat have revealed a comparatively restricted distribution of the NO synthetic enzyme, NO synthase (NOS-1). Recent physiological studies, however, have shown that NO-mimicking nitrovasodilators can alter intraocular pressure in monkeys through an action (at least in part) on outflow resistance. The current studies, which determine the sites of NO synthesis in the human outflow pathway, were performed to provide an anatomic and biochemical explanation for these observations. METHODS: The occurrence and distribution of sites of ocular NO production in postmortem human eyes were determined using the isozyme-independent NO-indicator marker, NADPH-diaphorase (NADPH-d), together with direct biochemical assay and immunocytochemical localization of specific NO synthase (NOS) isoforms. RESULTS: The ciliary muscle (CM) and outflow pathway of normal human eyes were found to be substantially enriched in NADPH-d, the majority of which, by immunological analysis, consisted not of NOS-1 (brain or bNOS) but rather of NOS type 3 (endothelial cell or ecNOS). Biochemical analysis confirmed the NADPH-dependent production of NO and, unlike the primarily soluble distribution of bNOS, activity was found in both particulate and soluble fractions. NO reactivity was enriched in major sites of outflow resistance (trabecular meshwork and Schlemm's canal) as well as in collecting channels and was particularly prominent in the CM, especially in the anatomically distinct longitudinal subgroup of CM fibers that insert near (and may normally play a role in regulating resistance in) the trabecular meshwork. CONCLUSION: The human outflow pathway and CM are enriched sites of NO synthesis. These sites are anatomically distributed in such a manner as to suggest that one possible role for NO in the anterior segment may be to modulate outflow resistance either directly at the level of the trabecular meshwork, Schlemm's canal and collecting channels, or indirectly through alteration in the tone of the longitudinal CM.

Adolescent↗
PubMed1992

Effect of hyaluronidase on aqueous outflow resistance in normotensive and glaucomatous eyes of dogs.

The anterior chambers in 16 dogs with normotensive eyes and 3 Beagles with glaucomatous eyes were treated with 0, 25, 50, or 100 IU of bovine testicular hyaluronidase. Aqueous outflow resistance was then determined by constant-pressure perfusion of 0.9% NaCl solution for 30 or 60 minutes. In normotensive eyes, 25, 50, or 100 IU of hyaluronidase significantly (P less than 0.02) increased the rate of constant-pressure perfusion compared with that of untreated eyes during 30- or 60-minute perfusions. Treatment of glaucomatous eyes with 25, 50, or 100 IU of hyaluronidase did not significantly increase the rate of constant-pressure perfusion over controls during a 30-minute perfusion. Bovine testicular hyaluronidase at all doses removed the staining of colloidal iron from the trabecular meshwork in normotensive eyes. In Beagles with glaucoma, the trabecular meshworks remained stained with colloidal iron when treated with the hyaluronidase, which suggested that some glycosaminoglycans were resistant to this enzyme's action.

Animals↗
PubMed1991

The choice of surgical procedure in congenital, infantile, and juvenile glaucoma.

1. Trabeculotomy is successful in patients with an angle anomaly involving only the trabecular meshwork, but in those involving the trabecular meshwork with iris or cornea, trabeculotomy combined with trabeculectomy is recommended. 2. In cases of failed trabeculotomy or trabeculectomy, a Molteno implant can be tried, although it does not work well in patients with congenital glaucoma. 3. If all else fails, a cyclodestructive procedure is indicated and contact Nd:YAG laser cyclophotocoagulation is recommended.

Child↗
PubMedDate not supplied

The choice of surgical procedure in congenital, infantile, and juvenile glaucoma.

Trabeculotomy is successful in patients with an angle anomaly involving only the trabecular meshwork, but in those involving the trabecular meshwork with iris and/or cornea trabeculotomy combined with trabeculectomy is recommended. In cases of failed trabeculotomy or trabeculectomy, a Molteno implant can be tried, although it does not work well in patients with congenital glaucoma. If all else fails, a cyclodestructive procedure is indicated and contact Nd:YAG laser cyclophotocoagulation is recommended.

Adolescent↗
PubMed1998

CD44H localization in primary open-angle glaucoma.

PURPOSE: Primary open-angle glaucoma (POAG) is associated with a decreased content of hyaluronan in the trabecular meshwork and in the juxtacanalicular connective tissue. In this study, the authors examined selected regions of the anterior segment to localize and determine the content of CD44H, a transmembrane multifunctional glycoprotein and the principal receptor of hyaluronan. METHODS: Sections of ethanol-fixed anterior segments of six POAG and six normal postmortem eyes were analyzed by immunostaining with and without the nonionic detergent Triton X-100, using the CD44H monoclonal antibody, and the avidin/biotin complex. They were visualized by Vector VIP substrate and were quantitated by computer-aided color image analysis. RESULTS: CD44H was expressed in all regions. Statistically significant decreased content of CD44H was observed in the POAG regions compared with normal regions--ciliary muscle (P < 0.001), ciliary stroma (P < 0.001), anterior iris (P < 0.05), iris root (P < 0.05), and trabecular meshwork (P < 0.05)--and in a subgroup of nonlaser POAG juxtacanalicular connective tissue (P < 0.05) and trabecular meshwork (P < 0.01). In sections treated with Triton X-100 a further increase in immunostaining was observed in normal eyes. As evidenced by scattergram plots of the ciliary body stroma region of the change in the optical density of CD44H between pretreatment with Triton X-100 and without Triton X-100 (y axis) versus the optical density of CD44H without Triton X-100 (x axis), individual cases of POAG were separated from normals. CONCLUSIONS: These results indicate that CD44H may represent a marker of POAG and an etiologic factor in the POAG disease process.

Aged↗
PubMed1995

Regulation of outflow rate and resistance in the perfused anterior segment of the bovine eye.

Contractile properties of isolated trabecular meshwork strips have recently been described. In the present paper we characterize the regulation of the outflow pathway in the isolated perfused anterior segment of the bovine eye. Anterior segments of bovine eyes with detached iris, ciliary body and ciliary muscle were perfused at constant pressure of 8.8 mmHg. A constant outflow of approximately 6-8 microliters min-1 could be obtained for at least 3 hr. The calculated outflow resistance was in the range 1.1-1.4 mmHg min microliter-1. The relative outflow was significantly reduced after application of carbachol, reaching a maximal inhibition of 30%. EC50 for carbachol was 3 x 10(-8) mol l-1. Atropin completely blocked the effect of carbachol on outflow. Morphological examination of perfused anterior segments which were perfused with carbachol revealed an intact fine structure of the meshwork cells. Pilocarpine at 10(-5) mol l-1 reduced outflow by 15%. Epinephrine at 10(-5) mol l-1 reduced outflow, while epinephrine at 10(-6) mol l-1 slightly increased the outflow rate. This effect could be blocked by metipranolol. Endothelin-1 in concentrations of 2 x 10(-9) and 2 x 10(-8) mol l-1 inhibited relative outflow by > 30%. Carbachol, pilocarpine, endothelin and a high dose of epinephrine, which have been shown to induce contractions in isolated bovine trabecular meshwork and ciliary muscle strips, induced a reduction of outflow rate and an increase of outflow resistance of the anterior segment. Thus, at least in the bovine eye, the trabecular meshwork per se is directly involved in the regulation of aqueous humor outflow.

Animals↗