Polarized Human Embryonic Stem Cell-Derived Retinal Pigment Epithelial Cell Monolayers Have Higher Resistance to Oxidative Stress-Induced Cell Death Than Nonpolarized Cultures

The capacity of S-Allylmercapto-N-acetylcysteine (ASSNAC) to protect human retinal pigment epithelial (RPE) cells (line ARPE-19) and porcine lenses from oxidative stress was studied. Confluent ARPE-19 cultures were incubated with ASSNAC or N-acetyl-cysteine (NAC) followed by exposure to oxidants and glutathione level and cell survival were determined. Porcine lenses were incubated with ASSNAC and then exposed to H2O2 followed by lens opacity measurement and determination of glutathione (reduced (GSH) and oxidized (GSSG)) in isolated lens adhering epithelial cells (lens capsule) and fiber cells consisting the lens cortex and nucleus (lens core). In ARPE-19 cultures, ASSNAC (0.2 mM; 24 h) increased glutathione level by 2–2.5-fold with significantly higher increase in GSH compared to NAC treated cultures. Similarly, ex-vivo exposure of lenses to ASSNAC (1 mM) significantly reduced the GSSG level and prevented H2O2 (0.5 mM)-induced lens opacification. These results demonstrate that ASSNAC up-regulates glutathione level in RPE cells and protects them from oxidative stress-induced cell death as well as protects lenses from oxidative stress-induced opacity. Further validation of these results in animal models may suggest a potential use for ASSNAC as a protective therapy in retinal degenerative diseases as well as in attenuation of oxidative stress-induced lens opacity.

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Collagen vitrigels with low‐fibril density enhance human embryonic stem cell‐derived retinal pigment epithelial cell maturation

Journal of Tissue Engineering and Regenerative Medicine ◽

10.1002/term.2598 ◽

2017 ◽

Vol 12 (3) ◽

pp. 821-829

Author(s):

Xiaokun Wang ◽

Julien Maruotti ◽

Shoumyo Majumdar ◽

Jose Roman ◽

Hai‐Quan Mao ◽

...

Keyword(s):

Stem Cell ◽

Epithelial Cell ◽

Embryonic Stem Cell ◽

Human Embryonic Stem Cell ◽

Retinal Pigment Epithelial ◽

Retinal Pigment Epithelial Cell ◽

Retinal Pigment ◽

Embryonic Stem ◽

Cell Maturation ◽

Pigment Epithelial

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Prevention of Oxidative Stress-Induced Retinal Pigment Epithelial Cell Death by the PPARγAgonist, 15-Deoxy-Delta 12, 14-ProstaglandinJ2

PPAR Research ◽

10.1155/2008/720163 ◽

2008 ◽

Vol 2008 ◽

pp. 1-7 ◽

Cited By ~ 13

Author(s):

Jason Y. Chang ◽

Puran S. Bora ◽

Nalini S. Bora

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Retinal Pigment Epithelial ◽

Retinal Pigment Epithelial Cell ◽

Retinal Pigment ◽

Age Related Macular Degeneration ◽

Experimental Conditions ◽

Pigment Epithelial ◽

Age Related ◽

Epithelial Cell Death

Cellular oxidative stress plays an important role in retinal pigment epithelial (RPE) cell death during aging and the development of age-related macular degeneration. Early reports indicate that during phagocytosis of rod outer segments, there is an increase of RPE oxidative stress and an upregulation of PPARγmRNA in these cells. These studies suggest that activation of PPARγmay modulate cellular oxidative stress. This paper presents a brief review of recent studies that investigate RPE oxidative stress under various experimental conditions. This is followed by a detailed review on those reports that examine the protective effect of the natural PPARγligand, 15d-PGJ2, against RPE oxidative stress. This agent can upregulate glutathione and prevent oxidant-induced intracellular reactive oxygen species accumulation, mitochondrial depolarization, and apoptosis. The cytoprotective effect of this agent, however, is not shared by other PPARγagonists. Nonetheless, this property of 15d-PGJ2may be useful in future development of pharmacological tools against retinal diseases caused by oxidative stress.

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