Cone Survival Despite Rod Degeneration in XOPS-mCFP Transgenic Zebrafish

Morris, Ann C.; Schroeter, Eric H.; Bilotta, Joseph; Wong, Rachel; Fadool, James M.

doi:10.1167/iovs.05-0797

Cited by 104 publications

(131 citation statements)

References 53 publications

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“…Cytoplasmic TUNEL labelling in Müller cells has been reported previously during normal vertebrate retinal development (Egensperger et al, 1996;Marín-Teva et al, 1999c;FranciscoMorcillo et al, 2004) and in the injured zebrafish retina (Morris et al, 2005;Thummel et al, 2008b;Bailey et al, 2010). Some authors claim that these TUNEL-positive Müller cells are apoptotic (Thummel et al, 2008b).…”

Section: Müller Cells In the Experimental Tench Retinal Tissuementioning

confidence: 77%

“…Some authors claim that these TUNEL-positive Müller cells are apoptotic (Thummel et al, 2008b). However, most of the studies cited above suggest that cytoplasmic TUNEL labelling results from the dispersion of photoreceptor DNA into the cytoplasm of Müller cells, which engulfed cell debris that originated during the degeneration process (Egensperger et al, 1996;Marín-Teva et al, 1999c;Francisco-Morcillo et al, 2004;Morris et al, 2005;Bailey et al, 2010). The apparent intact healthy morphology of Müller cells and the absence of apoptotic nuclei in the INL, in contrast with the strongly TUNEL-positive apoptotic bodies labelled in the ONL, support the second hypothesis.…”

Section: Müller Cells In the Experimental Tench Retinal Tissuementioning

confidence: 99%

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Light-induced degeneration and microglial response in the retina of an epibenthonic pigmented teleost: age-dependent photoreceptor susceptibility to cell death

Bejarano-Escobar

Blasco²,

Martı́n-Partido

et al. 2012

Journal of Experimental Biology

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SUMMARYConstant intense light causes apoptosis of photoreceptors in the retina of albino fish. However, very few studies have been performed on pigmented species. Tench (Tinca tinca) is a teleost inhabiting dimly lit environments that has a predominance of rods within the photoreceptor layer. To test the hypothesis that constant high intensity light can result in retinal damage in such pigmented epibenthonic teleost species, photodegeneration of the retina was investigated in the larvae and in juveniles of tench to assess whether any damage may also be dependent on fish age. We exposed both groups of animals to 5days of constant darkness, followed by 4days of constant 20,000lx light, and then by 6days of recovery in a 14h light:10h dark cycle. The results showed that the retina of the larvae group exhibited abundant photoreceptor cell apoptosis during the time of exposition to intense light, whereas that of juveniles was indifferent to it. Damaged retinas showed a strong TUNEL signal in photoreceptor nuclei, and occasionally a weak cytoplasmic TUNEL signal in Müller glia. Specific labelling of microglial cells with Griffonia simplicifolia lectin (GSL) histochemistry revealed that photoreceptor cell death alerts microglia in the degenerating retina, leading to local proliferation, migration towards the injured outer nuclear layer (ONL), and enhanced phagocytosis of photoreceptor debris. During the first days of intense light treatment, Müller cells phagocytosed dead photoreceptor cells but, once microglial cells became activated, there was a progressive increase in the phagocytic capacity of the microglia.

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Section: Müller Cells In the Experimental Tench Retinal Tissuementioning

confidence: 77%

Section: Müller Cells In the Experimental Tench Retinal Tissuementioning

confidence: 99%

Light-induced degeneration and microglial response in the retina of an epibenthonic pigmented teleost: age-dependent photoreceptor susceptibility to cell death

Bejarano-Escobar

Blasco²,

Martı́n-Partido

et al. 2012

Journal of Experimental Biology

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“…However, TUNEL analysis revealed a weak cytoplasmic signal in neuroepithelial cells near the SONCs, indicating that they also engulf cell debris, as has previously been described in our laboratory MartinPartido and Navascues, 1990). Similarly, TUNEL cytoplasmic labeling has also been detected in retinal Mü ller cells resulting from the ingestion of the fragmenting DNA from dying neighbor cells during normal development (Egensperger et al, 1996;Francisco-Morcillo et al, 2004) or under experimental conditions (Morris et al, 2005;Bailey et al, 2010).…”

Section: Spatiotemporal Distribution Of Cathepsin B/d-expressing Macrmentioning

confidence: 89%

Macrophage and microglia ontogeny in the mouse visual system can be traced by the expression of Cathepsins B and D

Bejarano-Escobar

Holguín-Arévalo

Montero

et al. 2011

Developmental Dynamics

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Here, we show a detailed chronotopographical analysis of cathepsin B and D expression during development of the mouse visual system. Both proteases were detected in large rounded/ameboid cells usually located in close relationship with prominent sites of extensive physiological cell death. In concordance with their morphological features and topographical distribution, we demonstrate that expressing cells corresponded with macrophages and microglial precursors. We found that as microglial precursors differentiated the expression of both cathepsins was down-regulated. Of interest, cathepsin B and D transcripts were never observed in degenerating cells. Our findings point to a role for cathepsin D and B in cell debris degradation after apoptotic processes rather than promoting cell death, as proposed for other developmental models. Additionally their pattern of expression suggests a role in the maturation of the microglial precursors.

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“…The identity of the proliferative cells identified in our preliminary study will require additional investigation. The availability of zebrafish mutations that cause rod degeneration (Morris et al, 2005), or all cone degeneration (this study), or selective cone type degeneration (Brockerhoff et al, 1997) as well as cell-selective ablation techniques (Davison et al, 2007;Pisharath et al, 2007), provide the opportunity to fine-tune our understanding of signals that induce proliferation and regulate cell fate determination.…”

Section: Discussionmentioning

confidence: 99%

A Mutation in the Cone-Specificpde6Gene Causes Rapid Cone Photoreceptor Degeneration in Zebrafish

Stearns¹,

Evangelista²,

Fadool³

et al. 2007

J. Neurosci.

110

129

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Photoreceptor degeneration is a common cause of inherited blindness worldwide. We have identified a blind zebrafish mutant with rapid degeneration of cone photoreceptors caused by a mutation in the cone phosphodiesterase c ( pde6c) gene, a key regulatory component in cone phototransduction. Some rods also degenerate, primarily in areas with a low density of rods. Rod photoreceptors in areas of the retina that always have a high density of rods are protected from degeneration. Our findings demonstrate that, analogous to what happens to rod photoreceptors in the rd1 mouse model, loss of cone phosphodiesterase leads to rapid degeneration of cone photoreceptors. Furthermore, we propose that cell density plays a key role in determining whether rod photoreceptors degenerate as a secondary consequence to cone degeneration. Our zebrafish mutant serves as a model for developing therapeutic treatments for photoreceptor degeneration in humans.

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Cone Survival Despite Rod Degeneration in XOPS-mCFP Transgenic Zebrafish

Cited by 104 publications

References 53 publications

Light-induced degeneration and microglial response in the retina of an epibenthonic pigmented teleost: age-dependent photoreceptor susceptibility to cell death

Light-induced degeneration and microglial response in the retina of an epibenthonic pigmented teleost: age-dependent photoreceptor susceptibility to cell death

Macrophage and microglia ontogeny in the mouse visual system can be traced by the expression of Cathepsins B and D

A Mutation in the Cone-Specificpde6Gene Causes Rapid Cone Photoreceptor Degeneration in Zebrafish

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