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, Weiye Li

Research output: Contribution to journalArticlepeer-review

Abstract

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 Müller cells in diabetic retina. Signaling pathways that are responsible for these Müller cell-mediated EPO/EpoR functions may be therapeutic targets for diabetic retinopathy.

Original languageEnglish (US)
Pages (from-to)1541-1555
Number of pages15
JournalFrontiers in Bioscience - Elite
Volume3 E
Issue number4
StatePublished - Jan 6 2011

Keywords

  • Diabetic retinopathy
  • Erythropoietin
  • Gliosis
  • MAPK/ERK
  • Müller cells
  • Neurotrophin
  • PI3K

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

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