Protection of RPE Cells from Oxidative Injury by 15-Deoxy-Δ<sup>12,14</sup>-Prostaglandin J<sub>2</sub>by Augmenting GSH and Activating MAPK

Qin, Suofu; McLaughlin, Anne; Vries, Gerald W. De

doi:10.1167/iovs.06-0318

Cited by 57 publications

(61 citation statements)

References 41 publications

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“…The sensitivity of cardiac myocytes to hydrogen peroxide was increased in MEKK1-negative cells (upstream of JNK), further suggesting the anti-apoptotic role of the JNK pathway (22). It has also been shown that the protective effect of cyclopentenone 15-deoxy-D12,14-prostaglandin J2 (dPGJ2), an endogenous PPARγ agonist that protects RPE cells from oxidative injury, is dependent on the activation of JNK and p38 (23). Thus, the JNK pathway is not simply a pro-or an anti-apoptotic pathway, which depends on cell and stimulus type, but requires co-activation of additional pathways and is also dependent on the duration of activation.…”

Section: Discussionmentioning

confidence: 99%

EGCG protects against UVB-induced apoptosis via oxidative stress and the JNK1/c-Jun pathway in ARPE19 cells

et al. 2011

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Abstract. Ultraviolet B (UVB) radiation is part of the spectrum of light produced by the sun. This form of radiation has been implicated as one of the potential etiological factors causing age-related macular degeneration (AMD). Oxidative injury to the retinal pigment epithelium (RPE) has also been thought to play a key role in AMD. The aim of the present study was to determine the mechanism by which UVB causes damage to the RPE cells, whether it occurs through oxidative stress and the mitogen-activated protein kinase (MAPK) pathway and whether the green tea extract, (-)-epigallocatechin gallate (EGCG), has a protective role. Cell viability assays were used to determine the viability of the cells under different conditions. Cell death caused by apoptosis was determined using fluorescein isothiocyanate conjugated-annexin V/PI labeling, followed by flow cytometry. Intracellular reactive oxygen species (ROS) levels were measured by flow cytometry. Western blot analysis was used to detect UVB-induced MAPK signaling pathways. The findings showed that UVB induced apoptosis, which increased intracellular ROS in ARPE19 cells. Inhibition of c-Jun NH2-terminal kinase (JNK) with a specific inhibitor augmented this apoptosis, and anisomycin (an activator of JNK) attenuated this apoptosis. In addition, UVB decreased the phosphorylation of JNK1 and c-Jun. Finally, EGCG reduced the ROS generation and apoptosis, and also partially blocked the decreased phosphorylation of JNK1 and c-Jun by UVB irradiation. The findings show that UVB irradiation is able to induce apoptosis in ARPE19 cells through oxidative stress, but EGCG treatment attenuates this damage. In this situation, the JNK pathway plays an anti-apoptotic role. The use of selective activators or antioxidants may be useful in reducing the oxidative damage occurring in AMD.

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Section: Discussionmentioning

confidence: 99%

EGCG protects against UVB-induced apoptosis via oxidative stress and the JNK1/c-Jun pathway in ARPE19 cells

et al. 2011

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“…Given the central role RPE plays in AMD pathogenesis, a commonly used experimental model to study the link between oxidative stress and AMD involves the use of cultured human RPE (ARPE-19) cells. Common endpoints include cell survival, morphology, activation of signaling cascades, and cytokine production (Chan et al, 2008;Dong et al, 2011;Glotin et al, 2006;Jiang et al, 2009;Klettner and Roider, 2009;Qin et al, 2006;Tsao et al, 2006;Wang et al, 1998;Wu et al, 2010).…”

Section: Age-related Macular Degenerationmentioning

confidence: 99%

“…In response to oxidants such as hydrogen peroxide or tert-butyl hydroperoxide, MAPK (most notably ERKs and p38 MAPK) activation has been shown to either protect against or exacerbate oxidative injury, differentiated by the amount of RPE cell death (Chan et al, 2008;Dong et al, 2011;Glotin et al, 2006;Jiang et al, 2009;Klettner and Roider, 2009;Qin et al, 2006;Tsao et al, 2006;Wang et al, 1998;Wu et al, 2010). These findings also raise questions as to the impact of oxidative stress on the outer BRB when the MAPK pathway is modulated pharmacologically by a MEK inhibitor.…”

Section: Mapk Activation and Oxidative Stress Response In The Retinamentioning

confidence: 99%

Retinal Vein Occlusion Induced by a MEK Inhibitor - Impact of Oxidative Stress on the Blood-Retinal Barrier

Yang¹,

Huang²

2012

Oxidative Stress and Diseases

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“…15d-PGJ2 possesses anti-inflammatory properties, and plays a protective role against oxidative stress both in vitro and in vivo (Giri et al, 2004;Itoh et al, 2004;Qin et al, 2006). Several studies have shown that 15d-PGJ2 affects the Nrf2-mediated transcription pathway.…”

Section: Introductionmentioning

confidence: 99%

15-Deoxy-prostaglandin J2 anti-inflammation in a rat model of chronic obstructive pulmonary disease and human bronchial epithelial cells via Nrf2 activation

Luo

Wang

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Nuclear factor-erythroid 2-related factor 2 (Nrf2) is a transcription factor that regulates antioxidant and anti-inflammatory genes, and it plays a crucial role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Moreover, 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2) plays a protective role against oxidative stress and inflammation both in vivo and in vitro. In a previous study, we found that 15d-PGJ2 increased the expression of Nrf2 in a COPD rat model. This study aims to elucidate the role of 15d-PGJ2 in COPD pathogenesis and the relationship between Nrf2 and human bronchial epithelial (HBE) cells. Normal HBE (HBE) cells were cultured. Following cigarette smoke extract (CSE) stimulation, pre-incubation with or without small interfering RNA (siRNA) Nrf2, and stimulation with or without 15d-PGJ2, the expression levels of Nrf2, NF-κBp65, and IL-8 were detected by reverse transcriptionpolymerase chain reaction and western blot, respectively. The expression of NF-κBp65 and IL-8 in CSE-stimulated normal HBE cells was inhibited by 15d-PGJ2 at both the mRNA level and the protein level. Moreover, the expression of Nrf2 in normal HBE cells was improved by 15d-PGJ2 at both the mRNA level and the protein level. However, the inhibitory or improving effects of 15d-PGJ2 were disengaged by siRNA Nrf2 at both the mRNA level and the protein level. 15d-PGJ2 possesses anti-inflammatory properties in the pathogenesis of COPD, and HBE cells stimulated by CSE via Nrf2 activation.

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Protection of RPE Cells from Oxidative Injury by 15-Deoxy-Δ^12,14-Prostaglandin J₂by Augmenting GSH and Activating MAPK

Abstract: Independent of its PPARgamma activity, dPGJ(2) protected cells from oxidative stress by elevating GSH and enhancing MAPK activation. Thus, dPGJ(2) may delay the development of dry-type age-related macular degeneration.

Cited by 57 publications

References 41 publications

EGCG protects against UVB-induced apoptosis via oxidative stress and the JNK1/c-Jun pathway in ARPE19 cells

EGCG protects against UVB-induced apoptosis via oxidative stress and the JNK1/c-Jun pathway in ARPE19 cells

Retinal Vein Occlusion Induced by a MEK Inhibitor - Impact of Oxidative Stress on the Blood-Retinal Barrier

15-Deoxy-prostaglandin J2 anti-inflammation in a rat model of chronic obstructive pulmonary disease and human bronchial epithelial cells via Nrf2 activation

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Protection of RPE Cells from Oxidative Injury by 15-Deoxy-Δ12,14-Prostaglandin J2by Augmenting GSH and Activating MAPK

Abstract: Independent of its PPARgamma activity, dPGJ(2) protected cells from oxidative stress by elevating GSH and enhancing MAPK activation. Thus, dPGJ(2) may delay the development of dry-type age-related macular degeneration.

Cited by 57 publications

References 41 publications

EGCG protects against UVB-induced apoptosis via oxidative stress and the JNK1/c-Jun pathway in ARPE19 cells

EGCG protects against UVB-induced apoptosis via oxidative stress and the JNK1/c-Jun pathway in ARPE19 cells

Retinal Vein Occlusion Induced by a MEK Inhibitor - Impact of Oxidative Stress on the Blood-Retinal Barrier

15-Deoxy-prostaglandin J2 anti-inflammation in a rat model of chronic obstructive pulmonary disease and human bronchial epithelial cells via Nrf2 activation

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Protection of RPE Cells from Oxidative Injury by 15-Deoxy-Δ^12,14-Prostaglandin J₂by Augmenting GSH and Activating MAPK