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

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          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 references 65

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          Molecular characterization of mitochondrial apoptosis-inducing factor.

          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

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              CD95's deadly mission in the immune system.

              Apoptosis in the immune system is a fundamental process regulating lymphocyte maturation, receptor repertoire selection and homeostasis. Thus, death by apoptosis is as essential for the function of lymphocytes as growth and differentiation. This article focuses on death receptor-associated apoptosis and the role of CD95 (Apo-1/Fas)-mediated signalling in T-cell and B-cell development and during the course of an immune response. Gaining an insight into these processes improves our understanding of the pathogenesis of diseases such as cancer, autoimmunity and AIDS, and opens new approaches to rational treatment strategies.

                Author and article information

                S. Karger AG
                July 2011
                22 July 2011
                : 226
                : Suppl 1
                : 10-17
                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
                328206 Ophthalmologica 2011;226(suppl 1):10–17
                © 2011 S. Karger AG, Basel

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                Page count
                Tables: 1, Pages: 8


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