Light-Induced Apoptosis in the Rat Retina in Vivo

Remé, Charlotte E.; Weller, Michael; Szczęsny, Piotr; Munz, K.; Hafezi, Farhad; Reinboth, Jörg-Joachim; Clausen, Matthias

doi:10.1007/978-1-4615-1897-6_3

Cited by 21 publications

(16 citation statements)

References 21 publications

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“…In vivo studies have shown that exposure of rats to constant light results in apoptosis of photoreceptor cells (25)(26)(27)(28)(29). Even moderate intensities of light exposure have been shown to damage the retinas of rats (30).…”

Section: Nuclear Factor-b (Nf-b)mentioning

confidence: 99%

Photo-oxidative Stress Down-modulates the Activity of Nuclear Factor-κB via Involvement of Caspase-1, Leading to Apoptosis of Photoreceptor Cells

Krishnamoorthy

Crawford

Chaturvedi³

et al. 1999

Journal of Biological Chemistry

120

107

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Section: Nuclear Factor-b (Nf-b)mentioning

confidence: 99%

Photo-oxidative Stress Down-modulates the Activity of Nuclear Factor-κB via Involvement of Caspase-1, Leading to Apoptosis of Photoreceptor Cells

Krishnamoorthy

Crawford

Chaturvedi³

et al. 1999

Journal of Biological Chemistry

120

107

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“…Recent studies have demonstrated a common pathway in several transgenic and naturally occurring animal models of these blinding diseases. In both inherited (2)(3)(4)(5) and light-induced (6)(7)(8) retinal degenerations, PRs die by apoptosis. These animal models correlate well with the pathology observed in human donor retinas affected with retinitis pigmentosa (9,10), and apoptosis in PRs has been seen in early stages of human retinitis pigmentosa (11).…”

mentioning

confidence: 99%

bcl-2 overexpression reduces apoptotic photoreceptor cell death in three different retinal degenerations.

Chen

Flannery

LaVail

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

190

108

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Apoptosis of photoreceptors occurs infrequently in adult retina but can be triggered in inherited and environmentally induced retinal degenerations. The protooncogene bcl-2 is knoWn to be a potent regulator of cell survival in neurons. We created lines oftransgenic mice overexpressing bcl-2 to test for its ability to increase photoreceptor survival. Bcl-2 increased photoreceptor survival in mice with retinal degeneration caused by a defective opsin or cGMP phosphodiesterase. Overexpression of Bcl-2 in normal photoreceptors also decreased the damaging effects of constant light exposure. Apoptosis was induced in normal photoreceptors by very high levels of bcl-2. We conclude that bcl-2 is an important regulator of photoreceptor cell death in retinal degenerations.

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“…1 Apoptosis is the mode of photoreceptor cell death in both human cases and animal models of RP and is now recognised as the final common pathway in many other human retinal disorders. 2 ± 5 Despite these observations the sequence of events that lead to photoreceptor apoptosis and the apoptotic pathways involved remain poorly characterised.…”

Section: Introductionmentioning

confidence: 99%

Caspase-independent photoreceptor apoptosis in vivo and differential expression of apoptotic protease activating factor-1 and caspase-3 during retinal development

2002

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Apoptosis is the mode of photoreceptor cell death in many retinal dystrophies. Exposure of Balb/c mice to excessive levels of light induces photoreceptor apoptosis and represents an animal model for the study of retinal degenerations. Caspases have emerged as central regulators of apoptosis, executing this tightly controlled death pathway in many cells. Previously we have reported that light-induced photoreceptor apoptosis occurs independently of one the key executioners of apoptosis, caspase-3. This present study extends these results reporting on the lack of activation of other caspases in this model including caspases-8, -9, -7, and -1. Furthermore, photoreceptor apoptosis cannot be inhibited with the broad range caspase inhibitor zVAD-fmk indicating that lightinduced retinal degeneration is caspase-independent. We demonstrate that cytochrome c does not translocate from mitochondria to the cytosol during photoreceptor apoptosis. We also show that during retinal development apoptotic protease activating factor (Apaf-1) protein levels are markedly decreased and this is associated with the inability to activate the mitochondrial caspase cascade in the mature retina. In addition, there is also a significant reduction in expression of caspases-3 and -9 during retinal maturation and these levels do not increase following light exposure. Finally, we show that the calcium-dependent proteases calpains are active during light-induced retinal degeneration and establish that the calcium channel blocker D-cis-diltiazem completely inhibits photoreceptor apoptosis.

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Light-Induced Apoptosis in the Rat Retina in Vivo

Cited by 21 publications

References 21 publications

Photo-oxidative Stress Down-modulates the Activity of Nuclear Factor-κB via Involvement of Caspase-1, Leading to Apoptosis of Photoreceptor Cells

Photo-oxidative Stress Down-modulates the Activity of Nuclear Factor-κB via Involvement of Caspase-1, Leading to Apoptosis of Photoreceptor Cells

bcl-2 overexpression reduces apoptotic photoreceptor cell death in three different retinal degenerations.

Caspase-independent photoreceptor apoptosis in vivo and differential expression of apoptotic protease activating factor-1 and caspase-3 during retinal development

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