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EPO reduces reactive gliosis and stimulates neurotrophin expression in Muller cells
Journal article   Open access   Peer reviewed

EPO reduces reactive gliosis and stimulates neurotrophin expression in Muller cells

Liu-Mei Hu, Yan Luo, Jingfa Zhang, Xia Lei, Jianfeng Shen, Yalan Wu, Mei Qin, Yaprak Banu Unver, Yong Zhong, Guo-Tong Xu, …
Frontiers in bioscience (Elite edition), v 3(4), pp 1541-1555
01 Jun 2011
DOI: https://doi.org/10.2741/e355
PMID: 21622158
url
https://doi.org/10.2741/e355View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze),  Open

Abstract

Animals Base Sequence Blotting, Western Cells, Cultured Diabetes Mellitus, Experimental - metabolism DNA Primers Down-Regulation Enzyme-Linked Immunosorbent Assay Erythropoietin - pharmacology Glial Fibrillary Acidic Protein - metabolism Gliosis - prevention & control Nerve Growth Factors - metabolism Polymerase Chain Reaction Rats Rats, Sprague-Dawley Retina - cytology Retina - drug effects Retina - metabolism Vimentin - metabolism
To characterize Müller cell-mediated neuroprotective and neurotrophic functions of the erythropoietin (EPO)/EPO receptor (EpoR) system in diabetic rat retina. A single intravitreal injection of EPO (8 mU/eye) was administered in rats 4 or 24 weeks after diabetes onset. The results showed that intravitreal EPO ameliorated the up-regulation of GFAP and vimentin in the diabetic retina evaluated by immunofluorescence and Western blotting; but up-regulated BDNF and CNTF expressions, quantified by real-time PCR and ELISA, in the 24-week diabetic rat retinas. In vitro, BDNF and CNTF expressions were stimulated by EPO through both extracellular signal-regulated kinase1/2 (ERK1/2) and Akt pathways. The neuro-regenerative function of EPO, as indicated by promotion of neurite outgrowth, was corroborated in vitro. BDNF was involved in EPO-induced neurite outgrowth of primary rat retinal neurons. Exogenous EPO exerts neuroprotective and neurotrophic functions by attenuating reactive gliosis and promoting neurotrophic factors in Muller cells in diabetic retina. Signaling pathways that are responsible for these Muller cell-mediated EPO/EpoR functions may be therapeutic targets for diabetic retinopathy.

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