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PubMed1996

Serum effects on aqueous outflow during anterior chamber perfusion in monkeys.

PURPOSE: To prevent the increase in outflow facility during anterior chamber perfusion in nonhuman primates by the addition of autologous serum to Bárány's mock aqueous humor. METHODS: Total outflow facility was measured simultaneously in both eyes of living cynomolgus monkeys for 3 hours by two-level constant pressure perfusion of the anterior chambers from elevated reservoirs with Bárány's solution with (one eye) or without (opposite eye) 3%, 5%, 10%, or 15% to 20% autologous serum. In other experiments, the anterior chamber contents initially were exchanged with Bárány's solution with (one eye) or without (opposite eye) 5% autologous serum, and the facility response to intravenous pilocarpine was determined. RESULTS: Eyes perfused with serum had a lower starting facility than control eyes, with facility decreasing with increasing serum concentrations. For both groups, facility increased with perfusion time and with volume of fluid perfused through the eye, but the rate of change of facility over time and per change in volume was significantly less for the serum-treated eyes. This difference remained significant when the proportional change of facility relative to baseline level was analyzed as a function of time but not as a function of volume. Intravenous infusion of pilocarpine increased facility by approximately the same proportion relative to baseline in both groups, but the absolute change and the final facility were lower in the serum-treated eyes. CONCLUSIONS: Serum or a serum component in the vicinity of the trabecular meshwork normally may help maintain outflow resistance but may be washed away during perfusion with serum-free media.

Animals↗
PubMed1996

Exfoliation syndrome.

Increasing pathophysiologic evidence indicates that exfoliation syndrome, a systemic process involving various visceral organs, frequently manifests itself first in the eyes as exfoliation of the lens and glaucoma. Exfoliation syndrome occurs when several tissues synthesize an abnormal basement membrane protein. This protein may obstruct the trabecular meshwork in the eye and cause glaucoma. We present a case of exfoliation syndrome associated with angle-closure glaucoma in a 57-year-old male patient from Taiwan. After peripheral iridectomy and topical antiglaucoma medications, intraocular pressure in both eyes was well controlled in the range of 15 to 20 mmHg. The mechanism of the glaucomatous optic neuropathy in this patient was probably caused by chronic angle-closure glaucoma superimposed with the exfoliation syndrome.

Antihypertensive Agents↗
PubMed1996

A gene for primary congenital glaucoma is not linked to the locus on chromosome 1q for autosomal dominant juvenile-onset open angle glaucoma.

BACKGROUND: Primary congenital glaucoma is an uncommon autosomal recessive condition that results from a developmental defect in the trabecular meshwork and anterior chamber angle, manifesting in the neonatal or infantile period with increased intraocular pressure, corneal enlargement and edema, and optic nerve cupping with consequent loss of vision. Nothing is known about its genetic location. PATIENTS AND METHODS: Linkage analysis was performed in 25 primary congenital glaucoma Saudi Arabian families with six polymorphic DNA markers on chromosome 1q in a region that has shown tight linkage to a locus for autosomal dominant juvenile-onset open angle glaucoma (GLC1A). Twenty-four of these families are highly consanguineous. RESULTS: Each family was shown separately to exclude the 8-centimorgan (cM) interval containing the GLC1A locus. Four families independently demonstrated overlapping regions of exclusion (theta < or = -2) that spanned the entire 8-cM interval. Assignment of a primary congenital glaucoma locus in this region could be excluded by a cadre of 21 families because a primary congenital glaucoma disease locus did not segregate in an autosomal recessive manner on haplotypes constructed with markers in this region. For all families, no affected individuals demonstrated homozygosity of alleles in regions tightly linked to the GLC1A locus. CONCLUSION: These results exclude the 8-cM region on chromosome 1q shown to contain the GLC1A locus from containing a disease locus for primary congenital glaucoma in this population of 25 Saudi Arabian families.

Chromosome Mapping↗
PubMed1977

The scleral spur and scleral roll.

The scleral spur and scleral roll together form a fibrous hoop which may be detached from adjacent structures as a unit. Tensile tests of the spur-roll resemble reported data on sclera. It is proposed that the circular structure of the spur-roll prevents action of the meridional portion of the ciliary muscle on the trabecular meshwork from collapsing the canal of Schlemm.

Aged↗
PubMed1997

Lack of association between hearing loss and glaucoma.

Some studies have suggested a relationship between glaucoma and sensorineural hearing loss. Others have found no evidence for an association. We performed a study to determine whether there is a significant difference in hearing between patients with glaucoma and a matched control population. Patients presenting themselves to a glaucoma clinic were grouped by type of glaucoma: uveitis, primary open-angle, pigmentary, pigmentary dispersion, congenital, or ocular hypertension. Patients older than 60 were excluded from the study, as were those who met certain carefully chosen exclusion criteria. Subjects included 40 men and 27 women, ranging in age from 15 to 60 years. Glaucoma was bilateral in all cases. Auditory thresholds at 0.5, 1.0, 2.0, and 3.0 kHz were measured bilaterally and statistically compared with American National Standards Institute (ANSI) normative values. Speech reception threshold and intelligibility were also assessed. When compared with speech ANSI values, there were no significant differences in mean thresholds at any frequency for any of the glaucoma types. Mean speech reception thresholds and intelligibility scores were all within normal limits and no subjects showed evidence of sensorineural hearing loss greater than expected for age. There were no differences between glaucoma groups, and we found no evidence of an association between glaucoma and hearing loss. There is disagreement about whether or not an association exists between glaucoma and hearing loss. Among those who do feel there is a relation, there is wide disagreement about what proportion of glaucomatous patients have a hearing loss. Rampoldi (1) first described an association between glaucoma and inner ear disease in 1889. Since that time, a number of reports have suggested such an association (2-4; 6-12). However, many of these studies are methodologically flawed. A few studies found no evidence of a relationship between glaucoma and sensorineural hearing loss (14, 15). There have been few reports since the 1970s, and the question remains unresolved. If there is, in fact, a relationship between glaucoma and inner ear disease, potentially much could be learned about certain forms of hearing loss from the study of glaucoma. In particular, surgical specimens (trabecular meshwork) could be obtained in those patients who undergo operations for their glaucoma. This tissue could be examined using current histopathological techniques. On the basis of the results, hypotheses might be made, by inference about which pathological processes are manifested in the inner ear. Therefore, we performed a study to evaluate whether there is a significant difference in hearing between patients with glaucoma and a matched control population.

Adolescent↗
PubMed1996

Hypothyroidism--a possible etiology of open-angle glaucoma.

BACKGROUND: Recent studies have shown an association between hypothyroidism and primary open-angle glaucoma (POAG). When hypothyroidism occurs, accumulation of hyaluronic acid within the trabecular meshwork may cause an increase in outflow resistance and intraocular pressure (IOP). This increase may be reversible with use of systemic treatment. METHODS: A hypothyroid patient is described whose IOP inversely varied with the use or the discontinuation of systemic hypothyroid medications. RESULTS: The patient's IOP was controlled when she complied with systemic treatment. CONCLUSIONS: In some cases, hypothyroidism may contribute to the genesis of open-angle glaucoma. Systemic treatment alone may be adequate to prevent progression of a glaucomatous diseased state. It may be prudent to investigate the presence of undiagnosed hypothyroidism in individuals with poorly controlled POAG, in individuals with normal-tension glaucoma, and in newly diagnosed cases.

Adult↗
PubMed1976

Centrioles and cilia in the mesothelial cells of the pericanalicular region.

An evaluation of 70 trabecular meshwork biopsies obtained at the time of therapeutic surgery in glaucomatous and cataractous eyes revealed that the mesothelial cells in the iridocorneal angle had a marked abundance of cilia and centrioles. The distribution of cells showing cilia and/or centrioles is positively correlated with the apparent aqueous humor outflow pathway. The morphology and arrangement of the cilia-centriole complexes in the angle are highly variable and show many forms not previously reported in a single tissue. There were no obvious correlations between organelle abundance and the identifiable factors affecting the patients involved in this study.

Biopsy↗
PubMed1976

[Contusion and luxation of the eyeball with rupture of the optic fascicle in fronto-basal trauma (author's transl)].

A report is given of the pathological changes in two eyes which were enucleated because of anterior luxation with rupture of the orbital optic nerve two hours after a traffic accident with frontal head injury. In the first case there was rupture of the trabecular meshwork and Schlemm's canal, the ciliary body and epithelium of the pars plana, a giant retinal tear at the ora serrata and a retinal avulsion at the optic disc, a partial rupture of the peripheral and a complete one of the central lamina cribrosa with a longitudinal tear in the optic nerve which lead to a complete rupture of the orbital optic nerve together with its sheats 22 mm behind the globe. The lesions produced arised probably from a slightly oblique course of the frontal trauma with a suggested additional rotating force followed by a sudden anterior movement of the eye with subsequent luxation. In the second case there was a giant tear at the ora serrata and at the pars plana with dislocation of unpigmented epithelium of the pars plana over the ciliary body, a rupture of the optic fascicle behind the lamina cribrosa, and a rupture of the optic dura mater 16.5 mm behind the globe.

Accidents, Traffic↗
PubMed1976

[Tonography after trabeculotomy (author's transl)].

In 25 eyes suffering from primary open angle glaucoma the facility of outflow was measured before and 1 to 3 months after surgery in consideration of the rigidity. Trabeculotomy improved the facility on an average of 0.14+/-0.02 to 0.28+/-0.03 units. This means that the outflow resistance is decreased from 10.58+/-1.34 to 4.31+/-0.45 units. The statistically highly significant improvement of the outflow conditions must be a consequence of the surgical opening in the trabecular meshwork as the sclera had been closed watertightly at the end of the trabeculotomy. The coefficient of rigidity (graphically determined by applanation tonometry and Schiötz tonometry in recumbent position) was decreased from 0.0208+/-0.0010 to 0.0172+/-0.0008. This means that measuring the intraocular pressure postoperatively with a Schiötz tonometer results in data which are 3.08+/-0.65 mm Hg lower than the actual pressure level.

Glaucoma↗
PubMed1998

GLC1A mutations point to regions of potential functional importance on the TIGR/MYOC protein.

PURPOSE: The aim of this study was to screen affected members of glaucoma families for mutations in the Trabecular Meshwork Inducible Glucocorticoid Response (TIGR) gene also known by the name myocilin (MYOC) or by combined names such as TIGR/MYOC. Our primary objectives were (1) to identify mutations responsible for glaucoma in members of three families for which we have shown linkage between chromosome 1 GLC1A-region markers and the primary open angle glaucoma (POAG) phenotype, and (2) to determine the relationship of these and other mutations to key points of predicted function and structure of the TIGR/MYOC protein. METHODS: DNA sequence determination was used to identify sequence changes in sections of the TIGR/MYOC gene that were PCR-amplified from genomic DNA from the probands of three previously-reported GLC1A juvenile-onset POAG families, UM:JG1, UM:JG3, UM:GL57, and unmapped family UM:JG5. Allele-specific oligonucleotide hybridization was used to screen for the identified mutations in PCR-amplified DNA from individual members of each pedigree and from a panel of 11 additional juvenile glaucoma family probands, 42 adult POAG family probands, and 43 normal individuals. Computerized algorithms were used to identify functional motifs and predict structures of normal and mutant forms of the protein. RESULTS: Sequence changes were found that alter amino acids in the olfactomedin-like domain near the carboxy terminal end of the TIGR protein in affected members of families UM:JG1 (Pro370Leu), UM:JG3 (Val426Phe), UM:GL57 (Glu323Lys) and UM:JG5 (Gly252Arg). Co-segregation of glaucoma and Pro370Leu, Val426Phe, and Gly252Arg in known GLC1A families suggests that these are mutations. Although the Gly252Arg substitution observed in UM:JG5 is non-conservative, it was not possible to distinguish whether it is a mutation or a polymorphism. None of the sequence changes described in these families were observed in other juvenile glaucoma cases in this study, nor in any of the POAG or phenotypically normal individuals tested here. Analysis of amino acid sequence changes resulting from mutations described in this and other works demonstrate localization of many mutations in the vicinity of predicted functional motifs in the olfactomedin-like domain. Identification of rat latrophilin (LPH1/CIRL) as a new member of the olfactomedin-like protein family to which TIGR/MYOC belongs suggests that the region of olfactomedin homology is a protein domain that can occur in different protein contexts. CONCLUSIONS: Location of mutations described in this and previous work suggests that some specific predicted protein motifs in the olfactomedin-like domain may be important to TIGR/MYOC function. In some cases, the role of TIGR/MYOC in the etiology of glaucoma may result from alteration of the sequences recognized by modifying enzymes such as casein kinase II. In other cases altered protein folding may affect access of enzymes to their target sequences on TIGR/MYOC. Although modifications and structures discussed here are predicted rather than proven, they provide a useful theoretical framework for design of subsequent experiments. Alterations to protein folding and predicted modification motifs cannot explain the pathogenic mechanisms of all of the known TIGR/MYOC glaucoma mutations.

Adult↗
PubMed2004

Intracellular sequestration of hetero-oligomers formed by wild-type and glaucoma-causing myocilin mutants.

PURPOSE: To investigate mechanism(s) by which mutations in the olfactomedin domain of myocilin (MYOC), also known as the trabecular meshwork-induced glucocorticoid response (TIGR) gene, cause autosomal dominant open-angle glaucoma, the structure and properties of wild-type (WT) MYOC protein were examined, when expressed alone or simultaneously with the Q368X or K423E disease-associated polypeptides. METHODS: Myocilin was analyzed in human aqueous humor and human trabecular meshwork (HTM) tissues. COS-7 and immortalized human trabecular meshwork (iHTM) cell lines were transfected with expression vectors encoding WT MYOC, mutated, and/or epitope-tagged cDNAs. MYOC proteins were characterized by double-epitope tagging procedures and/or Western blot analysis. RESULTS: MYOC polypeptides formed highly similar oligomers in aqueous humor, HTM tissues, transfected COS-7, and iHTM cell lines. These complexes ranged in size from 116 kDa to more than 200 kDa. The smallest complex, approximately 116 kDa, resulted from dimerization between two MYOC monomers. Expression of a 150-kDa complex was strongest in aqueous humor. Cotransfections of the WT construct with either the Q368X or K423E cDNA produced MYOC(WT)/MYOC(mutant) heterodimers and higher molecular weight hetero-oligomeric complexes. WT homo-oligomeric complexes were secreted in the extracellular media of both cell lines whereas the Q368X and K423E mutant/mutant homomultimers and heteromeric WT/mutant oligomers remained sequestered intracellularly. CONCLUSIONS: Formation of heteromeric WT/mutant complexes may provide a critical mechanism by which mutant myocilin polypeptides produce autosomal dominant open-angle glaucoma. The intracellular sequestration of abnormal WT/mutant complexes could lead to the malfunction of MYOC-expressing cells and to POAG potentially involving a dominant negative effect.

Animals↗
PubMed1984

Glaucoma in Sturge-Weber syndrome.

Trabeculectomy specimens from three eyes with Sturge-Weber syndrome were examined histopathologically. Changes in the trabecular meshwork-Schlemm's canal system were similar to findings in old age and in primary open-angle glaucoma. Two mechanisms for glaucoma are theorized. In cases with buphthalmos and congenital glaucoma, the chamber angle is often anomalous, as in other types of congenital glaucoma. In later onset juvenile cases, the chamber angle more often appears normal. A premature aging of the trabecular meshwork Schlemm's canal complex, as shown by us histopathologically, is a primary cause of juvenile glaucoma. It is suggested that both mechanisms relate to the abnormal hemodynamics of episclera and chamber angle, due to persistence of Streeter's primordial vascular plexus.

Angiomatosis↗
PubMed1997

Recurrent mutations in a single exon encoding the evolutionarily conserved olfactomedin-homology domain of TIGR in familial open-angle glaucoma.

Primary open-angle glaucoma (POAG) is a highly prevalent cause of irreversible blindness which associates cupping of the optic disc and alteration of the visual field, elevation of intraocular pressure being a major risk factor. Provided diagnosis is made at an early stage, treatments are available to prevent visual impairment. A locus, GLC1A, has been mapped on chromosome 1q23-q25 in several families affected with juvenile-onset POAG (JOAG) and also in some families affected with juvenile and middle-age onset POAG. Recently, three mutations of the TIGR (Trabecular meshwork-Induced Glucocorticoid Response) gene were shown to be responsible for the disease in several American families and in unrelated POAG patients. We now describe five new mutations in eight French families. All mutations known to date appear to concentrate in the evolutionarily conserved C-terminal domain of TIGR which bears homology to frog olfactomedin, an extracellular matrix glycoprotein of the olfactory epithelium, to rat and human neuronal olfactomedin-related proteins and to F11C3.2, a protein from Caenorhabditis elegans . Moreover, this conserved domain of TIGR is encoded by a single exon to which mutation screening could be limited. Surprisingly, the TIGR message, which is abundantly transcribed in the trabecular meshwork and also in the ciliary body and the sclera, is not expressed in the optic nerve whose degeneration is, however, the primary lesion of POAG.

Adolescent↗
PubMed2000

Immunohistochemical localization of MYOC/TIGR protein in the trabecular tissue of normal and glaucomatous eyes.

PURPOSE: To examine immunohistochemically the localization of myocilin/trabecular meshwork inducible glucocorticoid response (MYOC/TIGR) protein in the glaucomatous and normal trabecular meshworks. METHODS: Trabecular tissues were used from one eye with late-onset goniodysgenetic glaucoma, three with primary open angle glaucoma (one of which had the MYOC/TIGR gene mutation), two with exfoliation glaucoma and one without glaucoma. For light microscopic immunohistochemistry, frozen sections were stained by the avidin-biotin complex method using anti-MYOC/TIGR polyclonal antibody. For electron microscopic immunohistochemistry, the pre-embedding method using the same antibody was performed. Double immunostaining using both anti-MYOC/TIGR and anti-type VI collagen antibodies was done by the immunofluorescence method. RESULTS: With light microscopy, immunoreactivity was seen in the whole trabecular meshwork of each of the specimens. No notable differences were detected in staining among the types of glaucoma, or between the eyes with and those without the gene mutation. Under electron microscopy, immunoreaction products were observed not only in the cytoplasm of the trabecular cells but also in the extracellular matrix, where staining was associated with the long-spacing collagen, fine granular materials and possibly microfibrils. With double immunohistochemistry, MYOC/TIGR was colocalized with type VI collagen in the trabecular meshwork. CONCLUSIONS: In glaucomatous and normal trabecular meshworks, the MYOC/TIGR protein is distributed in the extracellular matrix colocalizing with type VI collagen.

Adolescent↗
PubMed1998

Molecular basis of open-angle glaucoma in Italy.

Glaucoma is a group of ocular diseases characterized by an optic neuropathy in which degeneration of retinal ganglion cells leads to a characteristic excavation of the optic nerve head. Primary open-angle glaucoma (POAG) can be subdivided into two groups according to age of onset:- 1. the more common middle- to late-age onset, chronic open-angle glaucoma (COAG) diagnosed after the age of 40 years; 2. the rarer juvenile open-angle glaucoma (JOAG), which is diagnosed between the age of 3 years and early adulthood. Recently, the gene coding for the trabecular meshwork-induced glucocorticoid response protein (TIGR), located in chromosome 1 (1q23-25), was found mutated in patients affected by POAG. In this work we describe the clinical and molecular genetic features of several Italian families affected by autosomal dominant POAG, collected in various regions of Italy.

Adult↗
PubMed2006

Evaluation of the anterior chamber angle in Asian Indian eyes by ultrasound biomicroscopy and gonioscopy.

PURPOSE: To compare the ultrasound biomicroscopic measurement of the anterior chamber angle in Asian Indian eyes, with the angle width estimated by gonioscopy. MATERIALS AND METHODS PARTICIPANTS: Patients with open and closed angles attending a glaucoma clinic were recruited for the study. OBSERVATION PROCEDURES: Temporal quadrants of the angles of patients were categorized by gonioscopy as Grade 0 to Grade 4, using Shaffer's classification. These angles were quantified by ultrasound biomicroscopy (UBM) using the following biometric characteristics: Angle opening distance at 250 micro (AOD 250) and 500 micro (AOD 500) from the scleral spur and trabecular meshwork-ciliary process distance (TCPD). The angles were further segregated as "narrow angles" (Schaffer's Grade 2 or less) and "open angles" (Schaffer's Grade 3 and 4). MAIN OUTCOME MEASURES: The UBM measurements were computed in each case and analyzed in relation to the gonioscopic angle evaluation. RESULTS: One hundred and sixty three eyes of 163 patients were analyzed. One hundred and six eyes had "narrow angles" and 57 eyes had "open angles" on gonioscopy. There was a significant difference among the mean UBM measurements of each angle grade estimated by gonioscopy (P < 0.001). The Pearson correlation coefficient between all UBM parameters and gonioscopy grades was significant at the 0.01 level. The mean AOD 250, AOD 500 and TCPD in narrow angles were 58+/-49 micro, 102+/-84 micro and 653+/-124 respectively, while it was 176+/-47 micro, 291+/-62 micro and 883+/-94 micro in eyes with open angles (P < 0.001) respectively. CONCLUSIONS: The angle width estimated by gonioscopy correlated significantly with the angle dimensions measured by UBM. Gonioscopy, though a subjective test, is a reliable method for estimation of the angle width.

Anterior Chamber↗
PubMed2000

Truncations in the TIGR gene in individuals with and without primary open-angle glaucoma.

PURPOSE: To investigate the coding exons in the trabecular meshwork-induced glucocorticoid response protein (TIGR) gene for mutations in primary open-angle glaucoma (POAG) in Chinese subjects. METHODS: Ninety-one Chinese patients with POAG and 113 of their family members without glaucoma were screened for sequence alterations in the TIGR gene by polymerase chain reaction, conformation-sensitive gel electrophoresis, and DNA sequencing. One hundred thirty-two unrelated individuals without glaucoma, aged 50 years or more, were studied as control subjects. RESULTS: Five sequence variants that lead to amino acid changes were identified. One was novel: Arg91Stop in one patient with POAG. Four had been reported: Arg46Stop in subjects with and without POAG, including an unaffected 77-year-old woman homozygous for Arg46Stop; Gly12Arg in subjects without glaucoma; and Asp208Glu and Thr353Ile in subjects with and without POAG. The previously reported 1-83(G-->A) and Arg76Lys polymorphisms were detected in both patients and controls and always occurred together. CONCLUSIONS: A different pattern of TIGR sequence variants exists in the Chinese than in non-Chinese populations. No common TIGR mutation that causes POAG was found. The occurrence of subjects without glaucoma who are heterozygous or homozygous for Arg46Stop suggests that reduction in the amount of TIGR protein does not cause glaucoma. Thus, the TIGR missense mutations known to cause POAG probably do not cause glaucoma by inactivating a normal TIGR function, but rather through the gain of a pathologic function.

Adolescent↗