Apoptosis in UV-exposed Rabbit Corneas

Podskochy, Alexander; Gan, Lisha; Fagerholm, Per

doi:10.1097/00003226-200001000-00019

Cited by 122 publications

(92 citation statements)

References 19 publications

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“…Podskochy et al (2000) have shown that UVB focused on the center of the un-wounded cornea of an anesthetized rabbit results in full thickness corneal damage with apoptosis of corneal epithelium, keratocytes, and corneal endothelial cells. Apoptosis of corneal epithelial cells, visualized by TUNEL staining and confirmed by electron microscopy, peaked at 24 hours post-UVR, as was seen in the current study; by 72 hours postexposure, keratocytes were completely absent from the exposed region of the cornea (Podskochy et al, 2000). By 7 days there was TOXICOLOGIC PATHOLOGY almost complete repopulation of the injured stroma by new keratocytes (Podskochy and Fagerholm, 1998).…”

Section: Discussionmentioning

confidence: 99%

Ultraviolet Radiation-Induced Corneal Degeneration in 129 Mice

et al. 2007

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Ultraviolet radiation (UVR) is a risk factor for the development of ocular disease in humans, including acute photokeratitis, chronic corneal spheroidal degeneration, and cataract formation. This report describes the ocular lesions seen in 21 mice chronically exposed to UVR as part of a skin carcinogenicity study. All globes were affected to varying degrees. The primary lesion, not previously reported in UVR-exposed mice, was marked loss of keratocytes relative to age-matched controls. Secondary lesions included corneal stromal thinning, keratoconus, corneal vascularization and fibrosis, keratitis, globe rupture, and phthisis bulbi. In addition, more than 90% of UVR-exposed and unexposed lenses had evidence of cataract formation; this is the first report of the occurrence of spontaneous cataracts in 129 mice. In a subsequent study, apoptotic cells were identified histologically and by cleaved caspase 3 immunoreactivity in the corneal epithelium and, less commonly, in the corneal stroma after acute UVR exposure. Based on this finding, we propose that the loss of keratocytes observed in the chronic study was due to UVR-induced apoptosis.

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Section: Discussionmentioning

confidence: 99%

Ultraviolet Radiation-Induced Corneal Degeneration in 129 Mice

et al. 2007

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“…There is definitive evidence that UV irradiation at wavelengths in the range from 280 to 310 nm induces apoptosis in the corneal epithelium based on terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL)-positive staining in the intact rabbit and rat corneas (Tronnier, 1980;Podskochy et al, 2000;. Recently, it has been shown that exposure to UV is the leading cause of post-PRK corneal epithelial detachment and death (Nagy et al, 1995(Nagy et al, ,1997Wilson, 1997;Johnson et al, 1998).…”

Section: Uv Irradiation-induced Cellular Damagementioning

confidence: 99%

“…6). In doing so the corneal epithelium and lens protect the retina from UV irradiation-induced damage (Ringvold, 1998;Taylor et al, 1998;Podskochy et al, 2000). In addition, repeated subthreshold or single threshold UV-exposures lead to inhibition of mitosis, nuclear fragmentation and loss of the whole corneal epithelial layer.…”

Section: Uv Irradiation-induced Cellular Damagementioning

confidence: 99%

Stress-induced corneal epithelial apoptosis mediated by K+ channel activation

2006

Progress in Retinal and Eye Research

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One of the functional roles of the corneal epithelial layer is to protect the cornea, lens and other underlying ocular structures from damages caused by environmental insults. It is important for corneal epithelial cells to maintain this function by undergoing continuous renewal through a dynamic process of wound healing. Previous studies in corneal epithelial cells have provided substantial evidence showing that environmental insults, such as ultraviolet (UV) irradiation and other biohazards, can induce stress-related cellular responses resulting in apoptosis and thus interrupt the dynamic process of wound healing. We found that UV irradiation-induced apoptotic effects in corneal epithelial cells are started by the hyperactivation of K + channels in the cell membrane resulting in a fast loss of intracellular K + ions. Recent studies provide further evidence indicating that these complex responses in corneal epithelial cells are resulted from the activation of stressrelated signaling pathways mediated by K + channel activity. The effect of UV irradiation on corneal epithelial cell fate shares common signaling mechanisms involving the activation of intracellular responses that are often activated by the stimulation of various cytokines. One piece of evidence for making this distinction is that at early times UV irradiation activates a Kv3.4 channel in corneal epithelial cells to elicit activation of c-Jun N-terminal kinase cascades and p53 activation leading to cell cycle arrest and apoptosis. The hypothetic model is that UV-induced potassium channel hyperactivity as an early event initiates fast cell shrinkages due to the loss of intracellular potassium, resulting in the activation of scaffolding protein kinases and cytoskeleton reorganizations. This review article presents important control mechanisms that determine Kv channel activity-mediated cellular responses in corneal epithelial cells, involving activation of stress-induced signaling pathways, arrests of cell cycle progression and/or induction of apoptosis.

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“…Indeed, the effect of UV light has been extensively investigated [1][2][3][4][5][6][7][8]. It has been reported that biotoxic epiphenomena may take place when the threshold level of radiation absorbed in corneal tissues is exceeded, and, consequently, permanent keratocyte damage or loss, epithelium destruction, endothelium edema and necrosis occur, as well as biochemical changes, such as ROS production, protein cross-linking, enzyme inactivation, DNA strand breaks and chemotactic factor release [9][10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Antioxidant protection in cultured corneal cells and whole corneas submitted to UV-B exposure

Ciuffi

Pisanello

Pagliai

et al. 2003

Journal of Photochemistry and Photobiology B: Biology

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Several corneal pathologies are characterized by the presence of reactive oxygen species (ROS); therefore, we evaluated the protection afforded by pirenoxine and melatonin to corneal cell culture and whole rabbit cornea from ultraviolet exposure and other oxidant systems.Rabbit cornea cell (SIRC) plates and whole corneas were exposed to UV-B (80 or 800 mJ/cm 2 ) or incubated with fMLPstimulated autologous macrophages, in the presence or absence of pirenoxine or melatonin (10 À5 M). The protective activity of compounds was assessed by measuring superoxide anion formation, inhibition of oxidation and mitochondrial viability. Moreover the ex vivo protective effect of pirenoxine and melatonin was verified in the whole cornea submitted to UV-B exposure in vitro.Our experimental data demonstrate that pirenoxine and melatonin were able to inhibit the superoxide formation and oxidative effect in cell culture and whole rabbit corneas submitted to UV-B exposure or to incubation with fMLP-stimulated autologous macrophages.Mitochondrial viability was restored in epithelial cells of rabbit cornea but not in SIRCs. Moreover, both compounds are also able to increase ex vivo epithelial corneal cell defences against the in vitro UV-B induced lipid peroxidation.

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Apoptosis in UV-exposed Rabbit Corneas

Abstract: Apoptosis appears to be a mechanism of corneal cell death after UVR. The 310-nm UVR caused more extensive damage to the corneal stroma and endothelium than did the 280-nm UVR.

Cited by 122 publications

References 19 publications

Ultraviolet Radiation-Induced Corneal Degeneration in 129 Mice

Ultraviolet Radiation-Induced Corneal Degeneration in 129 Mice

Stress-induced corneal epithelial apoptosis mediated by K+ channel activation

Antioxidant protection in cultured corneal cells and whole corneas submitted to UV-B exposure

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