Angiotensin II type 1 receptor blockade suppresses light-induced neural damage in the mouse retina

Narimatsu, Toshio; Ozawa, Yoko; Miyake, Seiji; Nagai, Norihiro; Tsubota, Kazuo

doi:10.1016/j.freeradbiomed.2014.03.020

Cited by 29 publications

(46 citation statements)

References 69 publications

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“…One source of oxidative stress can be light exposure; excessive light induces excessive activation of the visual cycle, which causes photoreceptor cell apoptosis. The role of oxidative stress in the mechanism was supported by previous findings that antioxidants, N-acetyl-L-cysteine (NAC) (Narimatsu et al, 2014) and lutein (Sasaki et al, 2012), can attenuate the apoptosis. Given that AMD is closely related to the condition of the retinal pigment epithelium (RPE) and choroid (Grisanti et al, 1997;Grisanti and Tatar, 2008), the influence of light exposure on the RPE-choroid is important in understanding the underlying mechanism of AMD pathogenesis (Ambati et al, 2003a).…”

Section: Introductionmentioning

confidence: 75%

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Blue light-induced inflammatory marker expression in the retinal pigment epithelium-choroid of mice and the protective effect of a yellow intraocular lens material in vivo

Narimatsu

Negishi

Miyake

et al. 2015

Experimental Eye Research

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Oxidative stress in the retinal pigment epithelium (RPE) is a well-accepted pathogenic change in vision-threatening diseases such as age-related macular degeneration. One source of oxidative stress is excessive light exposure, which causes excessive activation of the visual cycle. Because short wavelength light (blue light) has more energy, it is reported to be more harmful to photoreceptor cells than the other wavelengths of light. However, the biological effect of blue light in the RPE of living animals and the protective effect of a yellow intraocular lens (IOL) material that blocks blue light is still obscure. Therefore, we compared the pathogenic effect in the RPE-choroid complexes of mice exposed to light in a box made of a clear or a yellow IOL material. We measured the level of reactive oxygen species (ROS) using 2', 7'-dichlorodihydrofluorescein diacetate, the mRNA levels of inflammatory cytokines and a macrophage marker by real-time polymerase chain reaction, and the protein level of monocyte chemotactic protein-1 (MCP-1) by ELISA. The ROS level after light exposure was suppressed in the RPE-choroids of light-exposed mice in the yellow IOL material box. In parallel, all the inflammatory cytokines that we measured and a macrophage marker were also suppressed in the RPE-choroids of light-exposed mice in the yellow IOL material box. Therefore, a yellow IOL material suppressed, and thus blue light exacerbated, the increase in the ROS level and inflammatory cytokine expression as well as macrophage recruitment in the RPE-choroid in vivo after light exposure.

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Section: Introductionmentioning

confidence: 75%

“…Because light exposure increases the ROS level in the retina (Narimatsu et al, 2014), we first analyzed whether ROS levels were different in the RPE-choroids of the mice after exposure to light in the box made of clear or yellow IOL material (Fig. 1A).…”

Section: Introductionmentioning

confidence: 99%

Blue light-induced inflammatory marker expression in the retinal pigment epithelium-choroid of mice and the protective effect of a yellow intraocular lens material in vivo

Narimatsu

Negishi

Miyake

et al. 2015

Experimental Eye Research

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“…Therefore, we succeeded the induction of the retinal damage by 12 times lower intensity and 6 times shorter hours of blue LED exposure than the previous model. 19,21,22) While several studies reported that NAC protected against light-induced retinal damage, 13,14) no studies exist that that showed its protective effect in an in vivo model of LED light-induced retinal damage. In the present study, NAC was protective against murine blue LED light-induced retinal damage.…”

Section: Discussionmentioning

confidence: 99%

“…13,14) Electroretinogram Electroretinogram (ERG) was recorded on 5 d after blue LED light exposure. Mice were housed in a completely dark room for 24 h, followed by anesthesia with ketamine (120 mg/kg, intraperitoneally (i.p.…”

Section: Animalsmentioning

confidence: 99%

The Involvement of the Oxidative Stress in Murine Blue LED Light-Induced Retinal Damage Model

Nakamura

Kuse

Tsuruma

et al. 2017

Biological & Pharmaceutical Bulletin

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The aim of study was to establish a mouse model of blue light emitting diode (LED) light-induced retinal damage and to evaluate the effects of the antioxidant N-acetylcysteine (NAC). Mice were exposed to 400 or 800 lx blue LED light for 2 h, and were evaluated for retinal damage 5 d later by electroretinogram amplitude and outer nuclear layer (ONL) thickness. Additionally, we investigated the effect of blue LED light exposure on shorts-wave-sensitive opsin (S-opsin), and rhodopsin expression by immunohistochemistry. Blue LED light induced light intensity dependent retinal damage and led to collapse of S-opsin and altered rhodopsin localization from inner and outer segments to ONL. Conversely, NAC administered at 100 or 250 mg/kg intraperitoneally twice a day, before dark adaptation and before light exposure. NAC protected the blue LED light-induced retinal damage in a dose-dependent manner. Further, blue LED light-induced decreasing of S-opsin levels and altered rhodopsin localization, which were suppressed by NAC. We established a mouse model of blue LED light-induced retinal damage and these findings indicated that oxidative stress was partially involved in blue LED light-induced retinal damage.

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“…However, when ROS levels exceed processing capacity, they cause abnormal modifications of cellular components, such as proteins, and subsequently dysregulate multicellular organelles and induce cellular death [14]. Similarly, excessive light exposure increases ROS generation and causes retinal photoreceptor death [15, 16]. …”

Section: Introductionmentioning

confidence: 99%

Neuroprotective effect of bilberry extract in a murine model of photo-stressed retina

et al. 2017

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Excessive exposure to light promotes degenerative and blinding retinal diseases such as age-related macular degeneration and retinitis pigmentosa. However, the underlying mechanisms of photo-induced retinal degeneration are not fully understood, and a generalizable preventive intervention has not been proposed. Bilberry extract is an antioxidant-rich supplement that ameliorates ocular symptoms. However, its effects on photo-stressed retinas have not been clarified. In this study, we examined the neuroprotective effects of bilberry extract against photo-stress in murine retinas. Light-induced visual function impairment recorded by scotopic and phototopic electroretinograms showing respective rod and cone photoreceptor function was attenuated by oral administration of bilberry extract through a stomach tube in Balb/c mice (750 mg/kg body weight). Bilberry extract also suppressed photo-induced apoptosis in the photoreceptor cell layer and shortening of the outer segments of rod and cone photoreceptors. Levels of photo-induced reactive oxygen species (ROS), oxidative and endoplasmic reticulum (ER) stress markers, as measured by real-time reverse transcriptase polymerase chain reaction, were reduced by bilberry extract treatment. Reduction of ROS by N-acetyl-L-cysteine, a well-known antioxidant also suppressed ER stress. Immunohistochemical analysis of activating transcription factor 4 expression showed the presence of ER stress in the retina, and at least in part, in Müller glial cells. The photo-induced disruption of tight junctions in the retinal pigment epithelium was also attenuated by bilberry extract, repressing an oxidative stress marker, although ER stress markers were not repressed. Our results suggest that bilberry extract attenuates photo-induced apoptosis and visual dysfunction most likely, and at least in part, through ROS reduction, and subsequent ER stress attenuation in the retina. This study can help understand the mechanisms of photo-stress and contribute to developing a new, potentially useful therapeutic approach using bilberry extract for preventing retinal photo-damage.

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Angiotensin II type 1 receptor blockade suppresses light-induced neural damage in the mouse retina

Cited by 29 publications

References 69 publications

Blue light-induced inflammatory marker expression in the retinal pigment epithelium-choroid of mice and the protective effect of a yellow intraocular lens material in vivo

Blue light-induced inflammatory marker expression in the retinal pigment epithelium-choroid of mice and the protective effect of a yellow intraocular lens material in vivo

The Involvement of the Oxidative Stress in Murine Blue LED Light-Induced Retinal Damage Model

Neuroprotective effect of bilberry extract in a murine model of photo-stressed retina

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