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      Apoptosis and Other Cell Death Mechanisms after Retinal Detachment: Implications for Photoreceptor Rescue

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          Abstract

          Retinal detachment (RD) is one of the most common causes of blindness. This separation of the neurosensory retina from its underlying retinal pigment epithelium results in photoreceptor loss, which is the basis of permanent visual impairment. This review explores the various cell death mechanisms in photoreceptor death associated with RD. One of the major mechanisms is apoptosis, mediated by the intrinsic pathway, the Fas signalling pathway and/or the caspase-independent pathway. Other pathways of mechanisms include endoplasmic reticulum stress-mediated cell death, programmed necrosis and cytokine-related pathways. Understanding the mechanism of RD-associated photoreceptor death is likely to help us improve the current therapies or devise new strategies for this sight-threatening condition.

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          Most cited references65

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          Molecular characterization of mitochondrial apoptosis-inducing factor.

          S A Susin, H Lorenzo, N Zamzami … (1999)
          Mitochondria play a key part in the regulation of apoptosis (cell death). Their intermembrane space contains several proteins that are liberated through the outer membrane in order to participate in the degradation phase of apoptosis. Here we report the identification and cloning of an apoptosis-inducing factor, AIF, which is sufficient to induce apoptosis of isolated nuclei. AIF is a flavoprotein of relative molecular mass 57,000 which shares homology with the bacterial oxidoreductases; it is normally confined to mitochondria but translocates to the nucleus when apoptosis is induced. Recombinant AIF causes chromatin condensation in isolated nuclei and large-scale fragmentation of DNA. It induces purified mitochondria to release the apoptogenic proteins cytochrome c and caspase-9. Microinjection of AIF into the cytoplasm of intact cells induces condensation of chromatin, dissipation of the mitochondrial transmembrane potential, and exposure of phosphatidylserine in the plasma membrane. None of these effects is prevented by the wide-ranging caspase inhibitor known as Z-VAD.fmk. Overexpression of Bcl-2, which controls the opening of mitochondrial permeability transition pores, prevents the release of AIF from the mitochondrion but does not affect its apoptogenic activity. These results indicate that AIF is a mitochondrial effector of apoptotic cell death.
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            Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death

            Zoltán Oltval, Curt L. Milliman, Stanley Korsmeyer (1993)
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              ER stress and neurodegenerative diseases.

              D Lindholm, H Wootz, L Korhonen (2006)
              Endoplasmic reticulum (ER) stress is caused by disturbances in the structure and function of the ER with the accumulation of misfolded proteins and alterations in the calcium homeostasis. The ER response is characterized by changes in specific proteins, causing translational attenuation, induction of ER chaperones and degradation of misfolded proteins. In case of prolonged or aggravated ER stress, cellular signals leading to cell death are activated. ER stress has been suggested to be involved in some human neuronal diseases, such as Parkinson's disease, Alzheimer's and prion disease, as well as other disorders. The exact contributions to and casual effects of ER stress in the various disease processes, however, are not known. Here we will discuss the possible role of ER stress in neurodegenerative diseases, and highlight current knowledge in this field that may reveal novel insight into disease mechanisms and help to design better therapies for these disorders.
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                Author and article information

                Journal
                Journal ID (publisher-id): OPH
                Journal ID (nlm-ta): Ophthalmologica
                Journal ID (doi): 10.1159/issn.0030-3755
                Title: Ophthalmologica
                Publisher: S. Karger AG
                ISBN: 978-3-8055-9786-9
                ISBN: 978-3-8055-9787-6
                ISSN (Print): 0030-3755
                ISSN (Electronic): 1423-0267
                Publication date Subscription-year: 2011
                Publication date (Print): July 2011
                Publication date (Electronic): 22 July 2011
                Volume: 226
                Issue: Suppl 1
                Pages: 10-17
                Affiliations
                aEye Institute and bResearch Centre of Heart, Brain, Hormone and Healthy Ageing, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, SAR, China
                Author notes
                *Amy C.Y. Lo, Eye Institute, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, SAR (China), E-Mail amylo@hkucc.hku.hk
                Article
                Publisher ID: 328206 Other ID: Ophthalmologica 2011;226(suppl 1):10–17
                DOI: 10.1159/000328206
                PubMed ID: 21778775
                SO-VID: b674600e-fec1-440e-b507-d8d25a437c30
                Copyright © © 2011 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Page count
                Tables: 1, Pages: 8
                Categories
                Subject: Review

                ScienceOpen disciplines: Vision sciences,Ophthalmology & Optometry,Pathology
                Keywords: Caspase,Mitochondria,Neuroprotection,Necrosis,Programmed cell death
                Data availability:
                ScienceOpen disciplines: Vision sciences, Ophthalmology & Optometry, Pathology
                Keywords: Caspase, Mitochondria, Neuroprotection, Necrosis, Programmed cell death

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