Glaucoma: Thinking in new ways—a rôle for autonomous axonal self-destruction and other compartmentalised processes?

Whitmore, Alan V.; Libby, Richard T.; John, Simon W. M.

doi:10.1016/j.preteyeres.2005.04.004

Cited by 222 publications

(198 citation statements)

References 202 publications

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“…Despite the fact that the initial site of injury is unclear, glaucomatous neurodegeneration evidently exhibits widespread damage through a set of compartmentalized subcellular processes (Whitmore et al, 2005). Glaucomatous neurodegeneration eventually involves RGC soma and dendrites in the retina, axons in the optic nerve, and synapses in the brain.…”

Section: Evidence For Compartmentalized Processes Of Glaucomatous Neumentioning

confidence: 99%

Oxidative stress in glaucomatous neurodegeneration: Mechanisms and consequences

Tezel

2006

Progress in Retinal and Eye Research

600

449

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Reactive oxygen species (ROS) are generated as by-products of cellular metabolism, primarily in the mitochondria. Although ROS are essential participants in cell signaling and regulation, when their cellular production overwhelms the intrinsic antioxidant capacity, damage to cellular macromolecules such as DNA, proteins, and lipids ensues. Such a state of "oxidative stress" is thought to contribute to the pathogenesis of a number of neurodegenerative diseases. Growing evidence supports the involvement of oxidative stress as a common component of glaucomatous neurodegeneration in different subcellular compartments of retinal ganglion cells (RGCs). Besides the evidence of direct cytotoxic consequences leading to RGC death, it also seems highly possible that ROS are involved in signaling RGC death by acting as a second messenger and/or modulating protein function by redox modifications of downstream effectors through enzymatic oxidation of specific amino acid residues. Different studies provide cumulating evidence, which supports the association of ROS with different aspects of the neurodegenerative process. Oxidative protein modifications during glaucomatous neurodegeneration increase neuronal susceptibility to damage and also lead to glial dysfunction. Oxidative stress-induced dysfunction of glial cells may contribute to spreading neuronal damage by secondary degeneration. Oxidative stress also promotes the accumulation of advanced glycation end products in glaucomatous tissues. It is also evident that oxidative stress takes part in the activation of immune response during glaucomatous neurodegeneration, as ROS stimulate the antigen presenting ability of glial cells and also function as co-stimulatory molecules during antigen presentation. By discussing current evidence, this review provides a broad perspective on cellular mechanisms and potential consequences of oxidative stress in glaucoma.

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Section: Evidence For Compartmentalized Processes Of Glaucomatous Neumentioning

confidence: 99%

Oxidative stress in glaucomatous neurodegeneration: Mechanisms and consequences

Tezel

2006

Progress in Retinal and Eye Research

600

449

View full text Add to dashboard Cite

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“…Neurons have different types of self-destruct programs that are spatially compartmentalized, and one of these programs is located in the axon. Compartmentalized autonomous axonal selfdestruction has been proposed as an optic-nerve occurrence in glaucoma (Whitmore et al, 2005). Local noxae constricted to the prelaminar tissue would suffice to interrupt the continuity of axons.…”

Section: Introductionmentioning

confidence: 99%

Expression of Metabolic Coupling and Adhesion Proteins in the Porcine Optic-Nerve Head: Relevance to a Flow Model of Glaucoma

Carreras¹,

Porcel²,

Rodríguez-Hurtado³

et al. 2011

The Mystery of Glaucoma

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“…Recent work in the ageing and age related diseases such as glaucoma suggest that RGCs undergo a prolonged process of degeneration prior to elimination from the RGCL manifest as reduction in the complexity of the dendritic tree and the elimination of terminal processes (Watts et al, 2003;Whitmore et al, 2005;Williams et al, 2006;Kisiswa et al, 2009). These observations are consistent with those in other neuronal systems where parts of the neuron degenerate at different rates raising the possibility that during the early stages of degeneration, neuronal damage is associated with partial activation of programmed cell death (Whitmore et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, several groups have shown that caspase-independent cell death occurs in adult neurons (Okuno et al, 1998;Selznick et al, 2000;Zhang et al, 2002). Other types of cell death such as, autophagy, dark cell death and parapoptosis have been suggested to occur in glaucoma (Turmaine et al, 2000;Sperandio et al, 2004;Whitmore et al, 2005;Nixon, 2006;.…”

mentioning

confidence: 99%

Cellular inhibitor of apoptosis (cIAP1) is down-regulated during Retinal ganglion cell (RGC) maturation

Kisiswa

Albon

Morgan

et al. 2010

Experimental Eye Research

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Please cite this article as: Kisiswa, L., Albon, J., Morgan, J.E., Wride, M.A. Cellular inhibitor of apoptosis (cIAP1) is down-regulated during Retinal ganglion cell (RGC) maturation, Experimental Eye Research (2010Research ( ), doi: 10.1016Research ( /j.exer.2010 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. This work was supported by National Eye Research Centre (NERC), UK, Grant RCOP256. M A N U S C R I P T A C C E P T E D ACCEPTED MANUSCRIPT 2 AbstractApoptosis, is the main type of cell death that occurs in ageing and neurodegenerative disease, such as glaucoma. This study therefore characterises the expression profile of caspases (proapoptosis) and inhibitors of apoptosis (IAPs; anti-apoptosis) during maturation of the BrownNorway rat retina between 6 weeks and >24 weeks and also examines concomitant changes in expression of tumor necrosis factor receptor associated factor 2 (TRAF2). The expression profiles of caspases (initiator caspases 8, 9 and effector caspases 6, 7, 3) and inhibitors of apoptosis (IAPs) (Neuronal IAP), cellular IAP1 and 2 (cIAP1/2), X-chromosome linked IAP (XIAP), Survivin, Bruce and Livin) were examined in retinae from 6 weeks and >24 weeks old BN rats using semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), real-time PCR, Western blotting and immunofluoroscence analysis. Caspase expression was not altered significantly during the study interval. IAP expression showed a general reduction during maturation of BN retina, which was statistically significant for cIAP1. cIAP1 reduction was confirmed by Western blotting and immunoflouroscence and was restricted to cells in the retinal ganglion cell layer (RGCL). Accumulation of TRAF2 was observed in the RGCL accompanying the down-regulation of cIAP1 observed. Our results suggest that cells in the mature RGCL may have a greater susceptibility to cell death compared to their younger counterparts and this may be due in part to a reduction in activation of survival pathways involving IAPs and TRAFs.

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Glaucoma: Thinking in new ways—a rôle for autonomous axonal self-destruction and other compartmentalised processes?

Cited by 222 publications

References 202 publications

Oxidative stress in glaucomatous neurodegeneration: Mechanisms and consequences

Oxidative stress in glaucomatous neurodegeneration: Mechanisms and consequences

Expression of Metabolic Coupling and Adhesion Proteins in the Porcine Optic-Nerve Head: Relevance to a Flow Model of Glaucoma

Cellular inhibitor of apoptosis (cIAP1) is down-regulated during Retinal ganglion cell (RGC) maturation

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