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Role of the PNPLA2 Gene in the Regulation of Oxidative Stress Damage of RPE

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Retinal Degenerative Diseases

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 1185))

Abstract

Oxidative stress-mediated injury of the retinal pigment epithelium (RPE) can precede progressive retinal degeneration and ultimately lead to blindness (e.g., age-related macular degeneration (AMD)). The RPE expresses the PNPLA2 gene and produces its protein product PEDF-R that exhibits lipase activity. We have shown that transient PNPLA2 overexpression decreases dead-cell proteolytic activity and that synthetic peptides derived from a central region of PEDF-R efficiently protect ARPE-19 and pig primary RPE cells from oxidative stress. This study aims to evaluate the effect of loss of PNPLA2 in RPE cells undergoing oxidative stress. Loss of PNPLA2 conferred increased resistance to cells when subjected to oxidative stress.

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Acknowledgments

We thank Dr. Raul Heredia and Haley Haden for preparation of PNPLA2-silencing vectors. This work was supported by the Intramural Research Program of the NEI, NIH.

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Correspondence to S. Patricia Becerra .

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Subramanian, P., Becerra, S.P. (2019). Role of the PNPLA2 Gene in the Regulation of Oxidative Stress Damage of RPE. In: Bowes Rickman, C., Grimm, C., Anderson, R., Ash, J., LaVail, M., Hollyfield, J. (eds) Retinal Degenerative Diseases. Advances in Experimental Medicine and Biology, vol 1185. Springer, Cham. https://doi.org/10.1007/978-3-030-27378-1_62

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