The role of cell death during morphogenesis of the mammalian eye

Silver, Jerry; Hughes, Arthur

doi:10.1002/jmor.1051400204

Cited by 142 publications

(70 citation statements)

References 32 publications

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“…This decrease was more evident in the proximal pole of the cup (compare Fig. 6H,I with 6E,F) corresponding to the region where the optic fissure normally forms (Martín-Partido et al, 1988;Ozeki et al, 2000;Silver and Hughes, 1973). Altogether, these data indicate that Bmp7-mediated signalling controls proliferation and programmed cell death of RF precursors.…”

Section: Bmp7 Regulates Proliferation and Apoptosis During Optic Fissmentioning

confidence: 63%

Proper patterning of the optic fissure requires the sequential activity of BMP7 and SHH

et al. 2006

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The optic disc develops at the interface between optic stalk and retina, and enables both the exit of visual fibres and the entrance of mesenchymal cells that will form the hyaloid artery. In spite of the importance of the optic disc for eye function, little is known about the mechanisms that control its development. Here, we show that in mouse embryos, retinal fissure precursors can be recognised by the expression of netrin 1 and the overlapping distribution of both optic stalk (Pax2, Vax1) and ventral neural retina markers (Vax2, Raldh3). We also show that in the absence of Bmp7, fissure formation is not initiated. This absence is associated with a reduced cell proliferation and apoptosis in the proximoventral quadrant of the optic cup, lack of the hyaloid artery, optic nerve aplasia, and intra-retinal misrouting of RGC axons. BMP7 addition to organotypic cultures of optic vesicles from Bmp7 -/-embryos rescues Pax2 expression in the ventral region, while follistatin, a BMP7 antagonist, prevents it in early, but not in late, optic vesicle cultures from wild-type embryos. The presence of Pax2-positive cells in late optic cup is instead abolished by interfering with Shh signalling. Furthermore, SHH addition re-establishes Pax2 expression in late optic cups derived from ocular retardation (or) embryos, where optic disc development is impaired owing to the near absence of SHH-producing RGC. Collectively, these data indicate that BMP7 is required for retinal fissure formation and that its activity is needed, before SHH signalling, for the generation of PAX2-positive cells at the optic disc.

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Section: Bmp7 Regulates Proliferation and Apoptosis During Optic Fissmentioning

confidence: 63%

Proper patterning of the optic fissure requires the sequential activity of BMP7 and SHH

et al. 2006

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“…The area where apoptosis occurs in the ectoderm is annular in shape and circumscribes the region from which the lens will form. Later, at E12, apoptotic ectodermal cells are restricted to the boundary at which the lens vesicle is destined to separate from the surface ectoderm ( Figure 1C) and one can suggest that here, apoptosis has evolved as a means of dissociating the two tissues (Silver and Hughes, 1973).…”

Section: Programmed Cell Death During Early Eye Developmentmentioning

confidence: 97%

“…Pyknotic nuclei characteristic of apoptotic cells can be observed in the ventral wall of the optic stalk and in the presumptive lens ectoderm beginning at E11 in the rat (Figure 1) (Silver and Hughes, 1973). The dying cells observed in the optic cup do not die simultaneously but rather follow in temporal series from the disto-dorsal to the proximo-ventral pole of the eye rudiment.…”

Section: Programmed Cell Death During Early Eye Developmentmentioning

confidence: 97%

Apoptosis in mammalian eye development: lens morphogenesis, vascular regression and immune privilege

Lang

1997

Cell Death Differ

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Formation of the mammalian eye requires a complex series of tissue interactions that result in an organ of exquisite sensory capability. The early steps in eye development involve extensive cell death associated with morphogenesis. Later, suppression of programmed cell death is essential for tissue differentiation and in the adult, the immune privileged status of the eye is maintained in part through factors that induce inflammatory cell apoptosis. Experimental evidence suggests that suppression of apoptosis in cells of the lens lineage by fibroblast growth factors is one component of their action during lens morphogenesis. Fibroblast growth factors are also required for normal lens fiber-cell differentiation. This includes a degenerative step for organelles that is presumably an adaptation for the clearance of light scattering elements from the optic axis. The process of organelle degeneration may be related to apoptosis in a few of its features. Activelyinduced apoptosis becomes important for eye development as the temporary ocular vasculatures regress. This too, is presumably an adaptation for the disposal of cells that would disturb the passage of light to the retina. Ocular macrophages appear to be essential for the induction of apoptosis in the endothelial cells comprising the ocular vasculatures. In the adult, inflammatory cells entering the eye are exposed to the pro-apoptotic agents transforming growth factor-b2 and Fas ligand. The expression of these molecules in the eye, and their action in killing inflammatory cells, has evolved as a means of preventing inflammation and subsequent loss of vision. Thus, the eye offers a unique and versatile system for studying the role of programmed cell death in lens development, vascular regression and immune privilege.

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“…A more likely explanation is that the difference is due to the different ages examined in the two studies; our study examined animals at 6 weeks at the earliest stage and did not include animals as young as P6, where we would expect to see changes in caspase activity arising during development (Silver and Hughes, 1973;Silver and Robb, 1979).…”

Section: A C C E P T E D Accepted Manuscriptmentioning

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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The role of cell death during morphogenesis of the mammalian eye

Cited by 142 publications

References 32 publications

Proper patterning of the optic fissure requires the sequential activity of BMP7 and SHH

Proper patterning of the optic fissure requires the sequential activity of BMP7 and SHH

Apoptosis in mammalian eye development: lens morphogenesis, vascular regression and immune privilege

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

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