Long-term activation of c-Fos and c-Jun in optic nerve head astrocytes in experimental ocular hypertension in monkeys and after exposure to elevated pressure in vitro

2005 ◽  
Vol 1054 (2) ◽  
pp. 103-115 ◽  
Author(s):  
K. Hashimoto ◽  
A. Parker ◽  
P. Malone ◽  
B.T. Gabelt ◽  
C. Rasmussen ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Ocular Hypertension ◽  
Optic Nerve Head ◽  
Elevated Pressure

In vitro evaluation of reactive astrocyte migration, a component of tissue remodeling in glaucomatous optic nerve head

Glia ◽  
2001 ◽  
Vol 34 (3) ◽  
pp. 178-189 ◽  
Author(s):  
G�lg�n Tezel ◽  
M. Rosario Hernandez ◽  
Martin B. Wax
Keyword(s):  
Optic Nerve ◽  
Optic Nerve Head ◽  
Tissue Remodeling ◽  
Reactive Astrocyte ◽  
In Vitro Evaluation

scholarly journals Imaging video plethysmography shows reduced signal amplitude in glaucoma patients in the area of the microvascular tissue of the optic nerve head

2020 ◽  
Author(s):  
Ralf-Peter Tornow ◽  
Radim Kolar ◽  
Jan Odstrcilik ◽  
Ivana Labounkova ◽  
Folkert Horn
Keyword(s):  
Optic Nerve ◽  
Ocular Hypertension ◽  
Pulse Duration ◽  
Blood Volume ◽  
Optic Nerve Head ◽  
Light Absorption ◽  
Normal Subjects ◽  
Peak Amplitude ◽  
Time To Peak ◽  
Changing Light

Abstract Purpose To measure parameters of the cardiac cycle-induced pulsatile light absorption signal (plethysmography signal) of the optic nerve head (ONH) and to compare parameters between normal subjects and patients with different stages of glaucoma. Patients and methods A recently developed video ophthalmoscope was used to acquire short video sequences (10 s) of the ONH. After image registration and trend correction, the pulsatile changing light absorption at the ONH tissue (excluding large vessels) was calculated. The changing light absorption depends on the pulsatile changing blood volume. Various parameters, including peak amplitude, steepness, time-to-peak, full width at half maximum (FWHM), and pulse duration, were calculated for averaged individual pulses (heartbeats) of the plethysmography signal. This method was applied to 19 healthy control subjects and 91 subjects with ocular hypertension, as well as different stages of primary open-angle glaucoma (17 subjects with ocular hypertension, 24 with preperimetric glaucoma, and 50 with perimetric glaucoma). Results Compared to the normal subjects, significant reductions (p < 0.001) in peak amplitude and steepness were observed in the group of perimetric glaucoma patients, but no significant difference was found for time-to-peak, FWHM, and pulse duration. Peak amplitude and steepness showed high correlations with RNFL thickness (p < 0.001). Conclusions The presented low-cost video-ophthalmoscope permits measurement of the plethysmographic signal of the ONH tissue and calculation of different blood flow-related parameters. The reduced values of the amplitude and steepness parameters in perimetric glaucoma patients suggest decreased ONH perfusion and blood volume. This outcome is in agreement with results from other studies using OCT angiography and laser speckle flowgraphy, which confirm reduced capillary density in these patients. Registration site: www.clinicaltrials.gov, Trial registration number: NCT00494923

scholarly journals Longitudinal assessment of optic nerve head changes using optical coherence tomography in a primate microbead model of ocular hypertension

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Anita S. Y. Chan ◽  
Tin Aung Tun ◽  
John C. Allen ◽  
Myoe Naing Lynn ◽  
Sai Bo Bo Tun ◽  
...  
Keyword(s):  
Optical Coherence Tomography ◽  
Optic Nerve ◽  
Ocular Hypertension ◽  
Optic Nerve Head ◽  
Structural Damage ◽  
Structural Changes ◽  
Lamina Cribrosa ◽  
Optical Coherence ◽  
Longitudinal Assessment ◽  
The Mean

Abstract In humans, the longitudinal characterisation of early optic nerve head (ONH) damage in ocular hypertension (OHT) is difficult as patients with glaucoma usually have structural ONH damage at the time of diagnosis. Previous studies assessed glaucomatous ONH cupping by measuring the anterior lamina cribrosa depth (LCD) and minimal rim width (MRW) using optical coherence tomography (OCT). In this study, we induced OHT by repeated intracameral microbead injections in 16 cynomolgus primates (10 unilateral; 6 bilateral) and assessed the structural changes of the ONH longitudinally to observe early changes. Elevated intraocular pressure (IOP) in OHT eyes was maintained for 7 months and serial OCT measurements were performed during this period. The mean IOP was significantly elevated in OHT eyes when compared to baseline and compared to the control eyes. Thinner MRW and deeper LCD values from baseline were observed in OHT eyes with the greatest changes seen between month 1 and month 2 of OHT. Both the mean and maximum IOP values were significant predictors of MRW and LCD changes, although the maximum IOP was a slightly better predictor. We believe that this model could be useful to study IOP-induced early ONH structural damage which is important for understanding glaucoma pathogenesis.

scholarly journals DDIT3 (CHOP) contributes to retinal ganglion cell somal loss but not axonal degeneration in DBA/2J mice

2019 ◽  
Vol 5 (1) ◽  
Author(s):  
Olivia J. Marola ◽  
Stephanie B. Syc-Mazurek ◽  
Richard T. Libby
Keyword(s):  
Optic Nerve ◽  
Ocular Hypertension ◽  
Optic Nerve Head ◽  
Cellular Response ◽  
Molecular Mechanisms ◽  
Axonal Degeneration ◽  
Axonal Injury ◽  
Retinal Ganglion ◽  
Age Related

Abstract Glaucoma is an age-related neurodegenerative disease characterized by the progressive loss of retinal ganglion cells (RGCs). Chronic ocular hypertension, an important risk factor for glaucoma, leads to RGC axonal injury at the optic nerve head. This insult triggers molecularly distinct cascades governing RGC somal apoptosis and axonal degeneration. The molecular mechanisms activated by ocular hypertensive insult that drive both RGC somal apoptosis and axonal degeneration are incompletely understood. The cellular response to endoplasmic reticulum stress and induction of pro-apoptotic DNA damage inducible transcript 3 (DDIT3, also known as CHOP) have been implicated as drivers of neurodegeneration in many disease models, including glaucoma. RGCs express DDIT3 after glaucoma-relevant insults, and importantly, DDIT3 has been shown to contribute to both RGC somal apoptosis and axonal degeneration after acute induction of ocular hypertension. However, the role of DDIT3 in RGC somal and axonal degeneration has not been critically tested in a model of age-related chronic ocular hypertension. Here, we investigated the role of DDIT3 in glaucomatous RGC death using an age-related, naturally occurring ocular hypertensive mouse model of glaucoma, DBA/2J mice (D2). To accomplish this, a null allele of Ddit3 was backcrossed onto the D2 background. Homozygous Ddit3 deletion did not alter gross retinal or optic nerve head morphology, nor did it change the ocular hypertensive profile of D2 mice. In D2 mice, Ddit3 deletion conferred mild protection to RGC somas, but did not significantly prevent RGC axonal degeneration. Together, these data suggest that DDIT3 plays a minor role in perpetuating RGC somal apoptosis caused by chronic ocular hypertension-induced axonal injury, but does not significantly contribute to distal axonal degeneration.

The Association between Glaucomatous Visual Fields and Optic Nerve Head Features in the Ocular Hypertension Treatment Study

Ophthalmology ◽  
2006 ◽  
Vol 113 (9) ◽  
pp. 1603-1612 ◽  
Author(s):  
J KELTNER ◽  
C JOHNSON ◽  
D ANDERSON ◽  
R LEVINE ◽  
J FAN ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Ocular Hypertension ◽  
Optic Nerve Head ◽  
Visual Fields ◽  
Hypertension Treatment

scholarly journals Elevated hydrostatic pressure activates sodium/hydrogen exchanger-1 in rat optic nerve head astrocytes

2009 ◽  
Vol 297 (1) ◽  
pp. C111-C120 ◽  
Author(s):  
Amritlal Mandal ◽  
Mohammad Shahidullah ◽  
Nicholas A. Delamere ◽  
Marcos A. Terán
Keyword(s):  
Optic Nerve ◽  
Hydrostatic Pressure ◽  
Protein Expression ◽  
Optic Nerve Head ◽  
Elevated Hydrostatic Pressure ◽  
Cultured Astrocytes ◽  
Sodium Hydrogen Exchanger ◽  
Recovery From Acidification ◽  
Nhe1 Activity

Optic nerve head astrocytes become abnormal in eyes that have elevated intraocular pressure, and cultured astrocytes display altered protein expression after being subjected for ≥1 days to elevated hydrostatic pressure. Here we show that 2-h elevated hydrostatic pressure (15 or 30 mmHg) causes phosphorylation of ERK1/2, ribosomal S6 protein kinase (p90RSK), and Na/H exchanger (NHE)1 in cultured rat optic nerve head astrocytes as judged by Western blot analysis. The MEK/ERK inhibitor U0126 abolished phosphorylation of NHE1 and p90RSK as well as ERK1/2. To examine NHE1 activity, cytoplasmic pH (pHi) was measured with BCECF and, in some experiments, cells were acidified by 5-min exposure to 20 mM ammonium chloride. Although baseline pHi was unaltered, the rate of pHi recovery from acidification was fourfold higher in pressure-treated astrocytes. In the presence of either U0126 or dimethylamiloride (DMA), an NHE inhibitor, hydrostatic pressure did not change the rate of pHi recovery. The findings are consistent with NHE1 activation due to phosphorylation of ERK1/2, p90RSK, and NHE1 that occurs in response to hydrostatic pressure. These responses may precede long-term changes of protein expression known to occur in pressure-stressed astrocytes.

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