Free Radicals in Retinal Ischemia*

Bonne, C.; Müller, Agnès; Villain, Max

doi:10.1016/s0306-3623(97)00357-1

Cited by 138 publications

(74 citation statements)

References 46 publications

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“…5,6 Our present study demonstrated that H 2 O 2 -induced RGC death is attenuated in ASK1 KO mice in vitro ( Figure 7). Under stress conditions, several stress proteins, such as ubiquitin, play important roles as heat shock-and stress-regulated proteins.…”

Section: 30supporting

confidence: 55%

“…It has been proposed that free radicals are important mediators of damage caused by retinal ischemia. 5,6 Reperfusion injury after ischemia appears paradoxical, but oxygen-derived and other free radicals are principally formed when reduced compounds that accumulate during ischemia are reoxidized. 3 There is evidence that this free radical burst, produced during the early stage of reperfusion, overwhelms normal cellular antioxidant defense mechanisms, causing oxidative stress and a variety of types of tissue injury.…”

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confidence: 99%

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Role of Apoptosis Signal-Regulating Kinase 1 in Stress-Induced Neural Cell Apoptosis in Vivo

Harada

Nakamura

Namekata

et al. 2006

The American Journal of Pathology

104

107

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Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein kinase kinase kinase that plays an important role in oxidative stress-induced apoptosis. In the present study, we used ASK1 knockout (KO) mice to examine the possibility that ASK1 is involved in the neural cell apoptosis that occurs during retinal development and ischemic injury. ASK1 was expressed in retinal neurons, including retinal ganglion cells (RGCs), but retinal structure and extent of cell death during development were normal in ASK1 KO mice. On the other hand, the strain was less susceptible to ischemic injury, and the number of surviving retinal neurons was significantly increased compared with that in wild-type mice. Interestingly, ischemia-induced phosphorylation of p38 mitogen-activated protein kinase (p38), which mediates RGC apoptosis, was almost completely suppressed in ASK1 KO mice. In such retinas, the numbers of cleaved caspase-3-and TUNEL-positive neurons were apparently decreased compared with those in wild-type mice. Furthermore, cultured RGCs from ASK1 KO mice were resistant to H 2 O 2 -induced apoptosis. Our findings suggest that ASK1 is involved in the neural cell apoptosis after various kinds of oxidative stress. Thus, inhibition of the ASK1-p38 pathway could be useful for the treatment of neurodegenerative diseases including glaucoma. (Am J

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Section: 30supporting

confidence: 55%

mentioning

confidence: 99%

Role of Apoptosis Signal-Regulating Kinase 1 in Stress-Induced Neural Cell Apoptosis in Vivo

Harada

Nakamura

Namekata

et al. 2006

The American Journal of Pathology

104

107

View full text Add to dashboard Cite

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“…These include formation of reactive oxygen species (ROS), decrease in pH value, and changes in enzymatic activation, cytokine synthesis, gene activation and ionic concentration (Bonne et al, 1998;Kuriyama et al, 2001;Siskova and Wilhelm, 2001;Xu et al, 2004). Due to hypoxia, the ratio for the oxidative phosphorylation of adenosine diphosphate (ADP) to adenosine triphosphate (ATP) is changed as well.…”

Section: Flio In Retinal Artery Occlusionmentioning

confidence: 99%

Fluorescence lifetime imaging ophthalmoscopy

Dysli

Wolf

Zinkernagel

2017

Acta Ophthalmologica

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a b s t r a c tImaging techniques based on retinal autofluorescence have found broad applications in ophthalmology because they are extremely sensitive and noninvasive. Conventional fundus autofluorescence imaging measures fluorescence intensity of endogenous retinal fluorophores. It mainly derives its signal from lipofuscin at the level of the retinal pigment epithelium. Fundus autofluorescence, however, can not only be characterized by the spatial distribution of the fluorescence intensity or emission spectrum, but also by a characteristic fluorescence lifetime function. The fluorescence lifetime is the average amount of time a fluorophore remains in the excited state following excitation. Fluorescence lifetime imaging ophthalmoscopy (FLIO) is an emerging imaging modality for in vivo measurement of lifetimes of endogenous retinal fluorophores. Recent reports in this field have contributed to our understanding of the pathophysiology of various macular and retinal diseases.Within this review, the basic concept of fluorescence lifetime imaging is provided. It includes technical background information and correlation with in vitro measurements of individual retinal metabolites. In a second part, clinical applications of fluorescence lifetime imaging and fluorescence lifetime features of selected retinal diseases such as Stargardt disease, age-related macular degeneration, choroideremia, central serous chorioretinopathy, macular holes, diabetic retinopathy, and retinal artery occlusion are discussed. Potential areas of use for fluorescence lifetime imaging ophthalmoscopy will be outlined at the end of this review.

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“…The generation of reactive oxygen species (ROS), degradation of the antioxidant system, induction of cytokine production via transcriptional factors, and extracellular accumulation of glutamate that is excitotoxic to neuronal elements are the main alterations secondary to ischemia [1,16,18,19,34,38,40,41]. Reperfusion after initial ischemia paradoxically maintains the destruction process, perhaps due to increased levels of extracellular neurotransmitters, ROS, and waste products damaging previously unharmed cells when being reoxidized [1,5,28]. In this process, it is considered that xanthine oxidase (XO) is a major source of ROS [22,39].…”

Section: Introductionmentioning

confidence: 99%

Comparison of the Protective Effects of Prostaglandin Analogues in the Ischemia and Reperfusion Model of Rabbit Eyes

et al. 2009

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This study was planned to investigate the neuroprotective potentials of three commercially available prostaglandin analogues (PGA), in the ischemia and reperfusion model (I/R). Thirty New Zealand rabbits were divided into 5 groups and except for the control group (non-ischemic, non-treated), 0.9% NaCl, bimatoprost, latanoprost, or travoprost were applied to both eyes of animals of the respective groups for 1 week. At the end of treatment, ischemia was induced in both eyes of the 4 treatment groups by anterior chamber irrigation of the animals for 60 min. Following 24 h reperfusion, the animals were sacrified. Enucleated eyes and retinal tissues were investigated by light microscopy, electron microscopy, immunohistochemicstry for retinal histopathology, intracellular and apoptotic cells and by retinal morphometry. Vitreous samples were biochemically investigated for probable role of reactive oxygen species, by measuring xanthine oxidase (XO) activity. Analysis of morphometric measurements and vitreous XO activity revealed significant differences between the PGAtreated groups and the NaCl-treated group (P<0.05). Similarly, apoptotic cell counts in different retinal layers showed that PGA-treated groups had fewer apoptotic cells in all retinal layers than the NaCl-treated ischemic group (P<0.05). PGA may have high protective potential for different retinal layers and cells. Biochemical analysis of vitreous showed that all PGAs decreased vitreous XO activity significantly compared to the NaCl-treated group (P<0.05). However we could not find any statistically significant differences among the analogues. PGAs may reduce the injury induced by I/R, through the inhibition of XO activity, and it seems that their effects are elicited through numerous pathways.

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Free Radicals in Retinal Ischemia*

Cited by 138 publications

References 46 publications

Role of Apoptosis Signal-Regulating Kinase 1 in Stress-Induced Neural Cell Apoptosis in Vivo

Role of Apoptosis Signal-Regulating Kinase 1 in Stress-Induced Neural Cell Apoptosis in Vivo

Fluorescence lifetime imaging ophthalmoscopy

Comparison of the Protective Effects of Prostaglandin Analogues in the Ischemia and Reperfusion Model of Rabbit Eyes

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