Aqueous Neuroinflammatory Cytokines in Open Angle Glaucoma

2017 ◽  
Vol 68 (9) ◽  
pp. 2176-2180
Author(s):  
Anca Pantalon ◽  
Camelia Bogdanici ◽  
Daniela Constantinescu ◽  
Dorin Chiselita ◽  
Crengua Feraru
Keyword(s):  
Intraocular Pressure ◽  
Ganglion Cells ◽  
Open Angle Glaucoma ◽  
Vascular Dysfunction ◽  
Interleukin 1 ◽  
Field Testing ◽  
Interleukin 10 ◽  
Retinal Ganglion ◽  
Open Angle ◽  
Inflammatory Molecules

Typically in glaucoma the injuries in the retinal ganglion cells are irreversible and mostly due to high intraocular pressure. Currently there are also accepted pathogenic theories that go beyond high intraocular pressure in the area of neuro-inflammatory molecules, autoimmunity or vascular dysfunction. Yet it is very difficult to quantify these new pathogenic aspects as easy as in the case of visual field testing or optical coherence tomography. Our study tried to identify and compare levels of inflammatory cytokines IL-1Ra (Interleukin-1 receptor antagonist), IL-1a (Interleukin-1a), IL-1b (Interleukin-1b), IL-10 (Interleukin 10) and IFN-g(interferon-gamma) levels in open angle glaucoma and compare them to healthy subjects, matched for age and sex. The results proved an increased expression of inflammatory molecules with neurotoxicity capabilities in primary open angle glaucoma patients.

Effect of dietary modification and antioxidant supplementation on intraocular pressure and open-angle glaucoma

2020 ◽  
pp. 112067212096033 ◽  
Author(s):  
Sayena Jabbehdari ◽  
Judy L Chen ◽  
Thasarat Sutabutr Vajaranant
Keyword(s):  
Oxidative Stress ◽  
Intraocular Pressure ◽  
Vision Loss ◽  
Ganglion Cells ◽  
Open Angle Glaucoma ◽  
Cell Loss ◽  
Glaucomatous Optic Neuropathy ◽  
Retinal Ganglion ◽  
Open Angle ◽  
Modifiable Factor

Primary open-angle glaucoma (POAG) is an age-dependent, intraocular pressure (IOP)-related degeneration of the retinal ganglion cells (RGC). At present, IOP is the only modifiable factor that has been identified to prevent glaucomatous vision loss. Though the pathogenesis of glaucomatous optic neuropathy is still not well understood, increasing evidence suggests oxidative stress may contribute to the induction and progression of glaucoma. Furthermore, antioxidant use may be protective against glaucoma through various mechanisms, including reducing IOP, preserving vascular health, and preventing ganglion cell loss. This article provides a comprehensive review of the effect of oxidative stress, diet, and antioxidant therapy on IOP and open-angle glaucoma.

scholarly journals Impact of Visual Field Testing on Intraocular Pressure Change Trends in Healthy People and Glaucoma Patients

2020 ◽  
Vol 2020 ◽  
pp. 1-6 ◽  
Author(s):  
Mengwei Li ◽  
Bingxin Zheng ◽  
Qi Wang ◽  
Xinghuai Sun
Keyword(s):  
Intraocular Pressure ◽  
Visual Field ◽  
Repeated Measures ◽  
Healthy Subjects ◽  
Open Angle Glaucoma ◽  
Field Testing ◽  
Automated Perimetry ◽  
Open Angle ◽  
Standard Automated Perimetry ◽  
The Impact

Purpose. To compare the impact of visual field (VF) testing on intraocular pressure (IOP) change trends between healthy subjects and glaucoma patients. Methods. We recruited healthy volunteer subjects who did not have previous ocular diseases and open-angle glaucoma patients who were medically controlled well. IOP in both eyes of each participant was measured by using a noncontact tonometer at five time points: before, immediately after (0 minute), and 10, 30, and 60 minutes after the standard automated perimetry. Repeated measures ANOVA was used to analyze the effect of VF testing on IOP change trends in healthy and glaucoma eyes. Results. Forty healthy subjects (80 eyes) and 31 open-angle glaucoma patients (62 eyes) were included for the study. The baseline IOP of healthy and glaucoma eyes was 16.11 ± 3.01 mmHg and 15.78 ± 3.57 mmHg, respectively. After the VF testing, the IOP in healthy eyes was decreased by 1.5% at 0 minute, 6.5% at 10 minutes (P<0.001), 6.6% at 30 minutes (P<0.001), and 7.0% at 1 hour (P<0.001), indicating that this reduction was sustained for at least 1 hour. However, the IOP in glaucoma eyes was increased by 12.7% at 0 minute (P<0.001) and, then, returned towards initial values 1 hour after the VF testing. Conclusions. IOP change trends after VF field testing between healthy subjects and glaucoma patients were quite different. VF testing led to a mild and relatively sustained IOP decrease in healthy subjects, whereas IOP in open-angle glaucoma patients tended to significantly increase immediately after VF testing and, then, returned to pretest values after 1 hour. These findings indicate that the factors of VF testing should be considered in the clinical IOP measurements.

scholarly journals Neuroprotection in Glaucoma: Old and New Promising Treatments

2017 ◽  
Vol 2017 ◽  
pp. 1-19 ◽  
Author(s):  
Dario Rusciano ◽  
Salvatore Pezzino ◽  
Maria Giulia Mutolo ◽  
Rossella Giannotti ◽  
Aloisa Librando ◽  
...  
Keyword(s):  
Intraocular Pressure ◽  
Molecular Mechanisms ◽  
Primary Open Angle Glaucoma ◽  
Open Angle Glaucoma ◽  
Mechanical Damage ◽  
Retinal Ganglion ◽  
Open Angle ◽  
Efficacy And Safety ◽  
Negative Effects ◽  
Fiber Layer

Glaucoma is a major global cause of blindness, but the molecular mechanisms responsible for the neurodegenerative damage are not clear. Undoubtedly, the high intraocular pressure (IOP) and the secondary ischemic and mechanical damage of the optic nerve have a crucial role in retinal ganglion cell (RGC) death. Several studies specifically analyzed the events that lead to nerve fiber layer thinning, showing the importance of both intra- and extracellular factors. In parallel, many neuroprotective substances have been tested for their efficacy and safety in hindering the negative effects that lead to RGC death. New formulations of these compounds, also suitable for chronic oral administration, are likely to be used in clinical practice in the future along with conventional therapies, in order to control the progression of the visual impairment due to primary open-angle glaucoma (POAG). This review illustrates some of these old and new promising agents for the adjuvant treatment of POAG, with particular emphasis on forskolin and melatonin.

scholarly journals Some Aspects of Vascular Theory of Development and Progression of Primary Open-Angle Glaucoma (Literature Review). Part 1

2019 ◽  
Vol 16 (1) ◽  
pp. 12-18
Author(s):  
S. I. Makogon ◽  
A. S. Makogon
Keyword(s):  
Primary Open Angle Glaucoma ◽  
Ganglion Cells ◽  
Open Angle Glaucoma ◽  
Vascular Wall ◽  
Biologically Active ◽  
Retinal Ganglion ◽  
Open Angle ◽  
Hemostatic System ◽  
Plasma Proteolytic Systems ◽  
The Impact

The article presents a review of studies on various aspects of vascular theory of primary open-angle glaucoma (POAG) development and progression. The data of foreign and domestic scientists on the influence of hemodynamic disturbances in the glaucoma pathogenesis, including various levels: Central, regional and microcirculatory. Violations of the universal mechanism of vascular tone regulation, namely endothelial dysfunction are described. Vascular endothelium is a barrier between vascular wall and blood plasma. When the endothelium is damaged, its antithrombotic properties are transformed into a powerful prothrombotic potential. This leads to an imbalance between vasoconstrictors (endothelin) and vasodilators (nitric oxide). In addition, the release of biologically active substances with local neurotoxic effects. The authors noted an increase in the concentration of endothelin-1, studied its interaction with nitrogen oxide and considered its role in the occurrence of ischemia and the impact on the death of retinal ganglion cells. Scientists have noticed an increase in the level of Willebrand factor and increased platelet aggregation in patients with progressive glaucoma. As a possible cause of hemodynamic disturbances and glaucoma progression, the authors consider changes in blood rheological properties. In addition, the state of the three closely interacting components: the wall of blood vessels (primarily endothelium and subendothelial structures); cellular elements of blood (primarily platelets) and plasma proteolytic systems ensure the normal functioning of the hemostatic system. Changes in of these components state may affect the hemostatic system. Therefore, further study of various directions of vascular theory will help in understanding the etiopathogenesis of glaucoma.

scholarly journals Genomic Locus Modulating Corneal Thickness in the Mouse Identifies POU6F2 as a Potential Risk of Developing Glaucoma

2017 ◽  
Author(s):  
Rebecca King ◽  
Felix L. Struebing ◽  
Ying Li ◽  
Jiaxing Wang ◽  
Allison Ashley Koch ◽  
...  
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Retinal Ganglion Cells ◽  
Central Corneal Thickness ◽  
Primary Open Angle Glaucoma ◽  
Ganglion Cells ◽  
Open Angle Glaucoma ◽  
Corneal Thickness ◽  
Retinal Ganglion ◽  
Open Angle

AbstractPurpose: Central corneal thickness (CCT) is one of the most heritable ocular traits and it is also a phenotypic risk factor for primary open angle glaucoma (POAG). The present study uses the BXD Recombinant Inbred (RI) strains to identify novel quantitative trait loci (QTLs) modulating CCT in the mouse with the potential of identifying a molecular link between CCT and risk of developing POAG.Methods: The BXD RI strain set was used to define mammalian genomic loci modulating CCT, with a total of 818 corneas measured from 61 BXD RI strains (between 60-100 days of age). The mice were anesthetized and the eyes were positioned in front of the lens of the Phoenix Micron IV Image-Guided OCT system or the Bioptigen OCT system. CCT data for each strain was averaged and used to identify quantitative trait loci (QTLs) modulating this phenotype using the bioinformatics tools on GeneNetwork (www.genenetwork.org). The candidate genes and genomic loci identified in the mouse were then directly compared with the summary data from a human primary open-angle glaucoma (POGA) genome wide association study (NEIGHBORHOOD) to determine if any genomic elements modulating mouse CCT are also risk factors for POAG.Results: This analysis revealed one significant QTL on Chr 13 and a suggestive QTL on Chr 7. The significant locus on Chr 13 (13 to 19 Mb) was examined further to define candidate genes modulating this eye phenotype. For the Chr 13 QTL in the mouse, only one gene in the region (Pou6f2) contained nonsynonymous SNPs. Of these five nonsynonymous SNPs in Pou6f2, two resulted in changes in the amino acid proline which could result in altered secondary structure affecting protein function. The 7 Mb region under the mouse Chr 13 peak distributes over 2 chromosomes in the human: Chr 1 and Chr 7. These genomic loci were examined in the NEIGHBORHOOD database to determine if they are potential risk factors for human glaucoma identified using meta-data from human GWAS. The top 50 hits all resided within one gene (POU6F2), with the highest significance level of p = 10−6 for SNP rs76319873. POU6F2 is found in retinal ganglion cells and in corneal limbal stem cells. To test the effect of POU6F2 on CCT we examined the corneas of a Pou6f2-null mice and the corneas were thinner than those of wild-type littermates. In addition, these POU6F2 RGCs die early in the DBA/2J model of glaucoma than most RGCs.Conclusions: Using a mouse genetic reference panel, we identified a transcription factor, Pou6f2, that modulates CCT in the mouse. POU6F2 is also found in a subset of retinal ganglion cells and these RGCs are sensitive to injury.Authors SummaryGlaucoma is a complex group of diseases with several known causal mutations and many known risk factors. One well-known risk factor for developing primary open angle glaucoma is the thickness of the central cornea. The present study leverages a unique blend of systems biology methods using BXD recombinant inbred mice and genome-wide association studies from humans to define a putative molecular link between a phenotypic risk factor (central corneal thickness) and glaucoma. We identified a transcription factor, POU6F2, that is found in the developing retinal ganglion cells and cornea. POU6F2 is also present in a subpopulation of retinal ganglion cells and in stem cells of the cornea. Functional studies reveal that POU6F2 is associated the central corneal thickness and with susceptibility of retinal ganglion cells to injury.

scholarly journals Mutant Myocilin Nonsecretion In Vivo Is Not Sufficient To Cause Glaucoma

2006 ◽  
Vol 26 (22) ◽  
pp. 8427-8436 ◽  
Author(s):  
Douglas B. Gould ◽  
Mark Reedy ◽  
Lawriston A. Wilson ◽  
Richard S. Smith ◽  
Randy L. Johnson ◽  
...  
Keyword(s):  
Intraocular Pressure ◽  
Vision Loss ◽  
Ganglion Cells ◽  
Open Angle Glaucoma ◽  
Open Angle ◽  
Elevated Intraocular Pressure ◽  
Human Mutation ◽  
Different Strains ◽  
The Unfolded Protein Response

ABSTRACT Glaucoma is a leading cause of blindness, affecting over 70 million people worldwide. Vision loss is the result of death of the retinal ganglion cells. The best-known risk factor for glaucoma is an elevated intraocular pressure (IOP); however, factors leading to IOP elevation are poorly understood. Mutations in the MYOC gene are an important cause of open-angle glaucoma. Over 70 MYOC mutations have been identified, and they lead to approximately 5% of all primary open-angle glaucoma cases. Nevertheless, the pathogenic mechanisms by which these mutations elevate IOP are presently unclear. Data suggest that a dominant interfering effect of misfolded mutant MYOC molecules may be pathogenic. To test this hypothesis, we have generated mice carrying a mutant allele of Myoc that is analogous to a human mutation that leads to aggressive glaucoma in patients. We show that mutant MYOC is not secreted into the aqueous humor. Instead of being secreted, mutant MYOC accumulates within the iridocorneal angle of the eye, consistent with the behavior of abnormally folded protein. Surprisingly, the accumulated mutant protein does not activate the unfolded protein response and lead to elevated intraocular pressure or glaucoma in aged mice of different strains. These data suggest that production, apparent misfolding, and nonsecretion of mutant MYOC are not, by themselves, sufficient to cause glaucoma in vivo.

CITICOLINE APPLICATIONS AS A COMPLEX PRIMARY TREATMENT

2020 ◽  
Vol 6 (1) ◽  
pp. 18-22
Author(s):  
Kh. Abulkasimova ◽  
◽  
M. Karimova
Keyword(s):  
Retinal Ganglion Cells ◽  
Primary Open Angle Glaucoma ◽  
Ganglion Cells ◽  
Open Angle Glaucoma ◽  
Primary Treatment ◽  
Retinal Ganglion ◽  
Open Angle ◽  
Complex Therapy ◽  
Stabilizing Effect ◽  
Lipid Balance

This article is about primary open-angle glaucoma (POAG) which is a multifactorial degenerative disease that affects the optic nerve and subsequently leads to the loss of retinal ganglion cells (RGC) and their axons. Therefore, preparations with antioxidant and membrane-stabilizing effect, as well as ensuring restoration of lipid balance, are relevant in the complex therapy of POAG.

scholarly journals Loss of retinal ganglion cells in a new genetic mouse model for primary open‐angle glaucoma

2019 ◽  
Vol 23 (8) ◽  
pp. 5497-5507 ◽  
Author(s):  
Sabrina Reinehr ◽  
Dennis Koch ◽  
Maximilian Weiss ◽  
Franziska Froemel ◽  
Christina Voss ◽  
...  
Keyword(s):  
Mouse Model ◽  
Retinal Ganglion Cells ◽  
Primary Open Angle Glaucoma ◽  
Ganglion Cells ◽  
Open Angle Glaucoma ◽  
Retinal Ganglion ◽  
Open Angle ◽  
Genetic Mouse Model
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