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Neuroprotective role of erythropoietin by antiapoptosis in the retina

✍ Scribed by Hyewon Chung; Hyunju Lee; Folami Lamoke; William J. M. Hrushesky; Patricia A. Wood; Wan Jin Jahng

Publisher
John Wiley and Sons
Year
2009
Tongue
English
Weight
452 KB
Volume
87
Category
Article
ISSN
0360-4012

No coin nor oath required. For personal study only.

✦ Synopsis

Abstract

Erythropoietin (EPO) stimulates red blood cell production, in part by inhibiting apoptosis of the red blood cell precursors. The erythropoietic effects of EPO are circadian stage dependent. Retinal injury due to light occurs through oxidative mechanisms and is manifest by retinal and retinal pigment epithelium (RPE) cells apoptosis. The visual cycle might be circadian coordinated as a means of effectively protecting the retina from the detrimental effects of light‐induced, oxygen‐dependent, free radical–mediated damage, especially at the times of day when light is more intense. We show that the retinal expression of EPO and its receptor (EPOR), as well as subsequent Janus kinase 2 (Jak2) phosphorylations, are each tightly linked to a specific time after oxidative stress and in anticipation of daily light onset. This is consistent with physiological protection against daily light‐induced, oxidatively mediated retinal apoptosis. In vitro, we verify that EPO protects RPE cells from light, hyperoxia, and hydrogen peroxide–induced retinal cell apoptosis, and that these stimuli increase EPO and EPOR expression in cultured RPE cells. Together, these data support the premise that EPO and its EPOR interactions represent an important retinal shield from physiologic and pathologic light‐induced oxidative injury. © 2009 Wiley‐Liss, Inc.

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