Endogenous erythropoietin from astrocyte protects the oligodendrocyte precursor cell against hypoxic and reoxygenation injury

Shin Kato, Mineyoshi Aoyama, Hiroki Kakita, Hideki Hida, Ineko Kato, Tetsuya Ito, Tatenobu Goto, Mohamed H. Hussein, Kazunobu Sawamoto, Hajime Togari, Kiyofumi Asai

Research output: Contribution to journalArticle

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Abstract

The hypoxia-responsive cytokine erythropoietin (EPO) provides neuroprotective effects in the damaged brain during ischemic events and neurodegenerative diseases. The purpose of the present study is to evaluate the EPO/EPO receptor (EPOR) endogenous system between astrocyte and oligodendrocyte precursor cell (OPC) under hypoxia. We report here elevated EPO mRNA levels and protein release in cultured astrocytes following hypoxic stimulation by quantitative RT-PCR and ELISA. Furthermore, the EPOR gene expressions were detected in cultured OPCs as in astrocytes and microglias by quantitative RT-PCR. Cell staining revealed the EPOR expression in OPC. To evaluate the protective effect of endogenous EPO from astrocyte to OPCs, EPO/EPOR signaling was blocked by EPO siRNA or EPOR siRNA gene silencing in in vitro study. The suppression of endogenous EPO production in astrocytes by EPO siRNA decreased the protection to OPCs against hypoxic stress. Furthermore, OPC with EPOR siRNA had less cell survival after hypoxic/reoxygenation injury. This suggested that EPO/EPOR signaling from astrocyte to OPC could prevent OPC damage under hypoxic/reoxygenation condition. Our present finding of an interaction between astrocytes and OPCs may lead to a new therapeutic approach to OPCs for use against cellular stress and injury.

Original languageEnglish
Pages (from-to)1566-1574
Number of pages9
JournalJournal of Neuroscience Research
Volume89
Issue number10
DOIs
Publication statusPublished - 01-10-2011

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Oligodendroglia
Erythropoietin
Astrocytes
Erythropoietin Receptors
Wounds and Injuries
Small Interfering RNA
Cell Hypoxia
Polymerase Chain Reaction
Gene Silencing
Neuroprotective Agents
Neurodegenerative Diseases
Cell Survival
Enzyme-Linked Immunosorbent Assay
Staining and Labeling
Cytokines
Gene Expression
Messenger RNA
Brain
Proteins

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience

Cite this

Kato, Shin ; Aoyama, Mineyoshi ; Kakita, Hiroki ; Hida, Hideki ; Kato, Ineko ; Ito, Tetsuya ; Goto, Tatenobu ; Hussein, Mohamed H. ; Sawamoto, Kazunobu ; Togari, Hajime ; Asai, Kiyofumi. / Endogenous erythropoietin from astrocyte protects the oligodendrocyte precursor cell against hypoxic and reoxygenation injury. In: Journal of Neuroscience Research. 2011 ; Vol. 89, No. 10. pp. 1566-1574.
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Kato, S, Aoyama, M, Kakita, H, Hida, H, Kato, I, Ito, T, Goto, T, Hussein, MH, Sawamoto, K, Togari, H & Asai, K 2011, 'Endogenous erythropoietin from astrocyte protects the oligodendrocyte precursor cell against hypoxic and reoxygenation injury', Journal of Neuroscience Research, vol. 89, no. 10, pp. 1566-1574. https://doi.org/10.1002/jnr.22702

Endogenous erythropoietin from astrocyte protects the oligodendrocyte precursor cell against hypoxic and reoxygenation injury. / Kato, Shin; Aoyama, Mineyoshi; Kakita, Hiroki; Hida, Hideki; Kato, Ineko; Ito, Tetsuya; Goto, Tatenobu; Hussein, Mohamed H.; Sawamoto, Kazunobu; Togari, Hajime; Asai, Kiyofumi.

In: Journal of Neuroscience Research, Vol. 89, No. 10, 01.10.2011, p. 1566-1574.

Research output: Contribution to journalArticle

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AU - Kato, Shin

AU - Aoyama, Mineyoshi

AU - Kakita, Hiroki

AU - Hida, Hideki

AU - Kato, Ineko

AU - Ito, Tetsuya

AU - Goto, Tatenobu

AU - Hussein, Mohamed H.

AU - Sawamoto, Kazunobu

AU - Togari, Hajime

AU - Asai, Kiyofumi

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N2 - The hypoxia-responsive cytokine erythropoietin (EPO) provides neuroprotective effects in the damaged brain during ischemic events and neurodegenerative diseases. The purpose of the present study is to evaluate the EPO/EPO receptor (EPOR) endogenous system between astrocyte and oligodendrocyte precursor cell (OPC) under hypoxia. We report here elevated EPO mRNA levels and protein release in cultured astrocytes following hypoxic stimulation by quantitative RT-PCR and ELISA. Furthermore, the EPOR gene expressions were detected in cultured OPCs as in astrocytes and microglias by quantitative RT-PCR. Cell staining revealed the EPOR expression in OPC. To evaluate the protective effect of endogenous EPO from astrocyte to OPCs, EPO/EPOR signaling was blocked by EPO siRNA or EPOR siRNA gene silencing in in vitro study. The suppression of endogenous EPO production in astrocytes by EPO siRNA decreased the protection to OPCs against hypoxic stress. Furthermore, OPC with EPOR siRNA had less cell survival after hypoxic/reoxygenation injury. This suggested that EPO/EPOR signaling from astrocyte to OPC could prevent OPC damage under hypoxic/reoxygenation condition. Our present finding of an interaction between astrocytes and OPCs may lead to a new therapeutic approach to OPCs for use against cellular stress and injury.

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