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Conference Paper: Peroxynitrite could regulate proliferation and neuronal differentiation of neural stem/progenitor cells through activating WNT/β-catenin signaling pathway

TitlePeroxynitrite could regulate proliferation and neuronal differentiation of neural stem/progenitor cells through activating WNT/β-catenin signaling pathway
Authors
Issue Date2014
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/jns
Citation
The 21st World Congress of Neurology (WCN 2013), Vienna, Austria, 20-26 September 2013. In Journal of the Neurological Sciences, 2013, v. 333 n. Suppl. 1, p. e228 How to Cite?
AbstractBackground: Hypoxia/ischemia could mediate the differentiation of neural stem/progenitor cells (NSCs) into mature neurons. In hypoxic/ischemic brain, nitric oxide and superoxide are simultaneously produced and they rapidly react to form peroxynitrite. Whether peroxynitrite can regulate neurogenesis is unknown yet. Objectives: Present study aims to understand the roles of peroxynitrite in regulating self-renewal, proliferation and differentiation of NSCs. Materials and methods: Primary cultured NSCs were subjected to different stimulations including peroxynitrite donor SIN-1, synthesized peroxynitrite and hypoxia treatment. For visualizing the formation of peroxynitrite, we developed a highly sensitive and specific fluorescent probe and detected the formation of peroxynitrite in the NSCs. We applied different biomarkers including Ki67, BrdU, Tuj1 and DCX, etc./INS; to identify the self-renewal proliferation, and neuronal differentiation of NSCs respectively. Results: Low concentrations of extraneous peroxynitrite (< 1 μM) promoted NSC/INS; proliferation, self-renewal and neuronal differentiation but high level of peroxynitrite (> 5 μM) induced cytotoxicity. Hypoxic treatment induced the production of peroxynitrite and promoted NSC/INS; proliferation and self-renewal, and neuronal differentiation. Treatments of peroxynitrite decomposition catalysts (PDCs, FeTMPyP and FeTPPS) reduced hypoxia-induced peroxynitrite formation, NSC/INS; proliferation, self-renewal and neuronal differentiation. The neurogenesis promoting effects were partly mediated through activating Wnt/β-catenin signaling pathway. Conclusion: Low concentration of peroxynitrite may serve as a cellular signaling for promoting NSC/INS; proliferation, self-renewal and neuronal differentiation. Copyright © 2013 Published by Elsevier B.V.
DescriptionConference Theme: Neurology in the Age of Globalization
Persistent Identifierhttp://hdl.handle.net/10722/201702
ISSN
2015 Impact Factor: 2.126
2015 SCImago Journal Rankings: 1.024

 

DC FieldValueLanguage
dc.contributor.authorShen, Jen_US
dc.contributor.authorChen, XM-
dc.contributor.authorYan, TT-
dc.date.accessioned2014-08-21T07:37:37Z-
dc.date.available2014-08-21T07:37:37Z-
dc.date.issued2014en_US
dc.identifier.citationThe 21st World Congress of Neurology (WCN 2013), Vienna, Austria, 20-26 September 2013. In Journal of the Neurological Sciences, 2013, v. 333 n. Suppl. 1, p. e228en_US
dc.identifier.issn0022-510X-
dc.identifier.urihttp://hdl.handle.net/10722/201702-
dc.descriptionConference Theme: Neurology in the Age of Globalization-
dc.description.abstractBackground: Hypoxia/ischemia could mediate the differentiation of neural stem/progenitor cells (NSCs) into mature neurons. In hypoxic/ischemic brain, nitric oxide and superoxide are simultaneously produced and they rapidly react to form peroxynitrite. Whether peroxynitrite can regulate neurogenesis is unknown yet. Objectives: Present study aims to understand the roles of peroxynitrite in regulating self-renewal, proliferation and differentiation of NSCs. Materials and methods: Primary cultured NSCs were subjected to different stimulations including peroxynitrite donor SIN-1, synthesized peroxynitrite and hypoxia treatment. For visualizing the formation of peroxynitrite, we developed a highly sensitive and specific fluorescent probe and detected the formation of peroxynitrite in the NSCs. We applied different biomarkers including Ki67, BrdU, Tuj1 and DCX, etc./INS; to identify the self-renewal proliferation, and neuronal differentiation of NSCs respectively. Results: Low concentrations of extraneous peroxynitrite (< 1 μM) promoted NSC/INS; proliferation, self-renewal and neuronal differentiation but high level of peroxynitrite (> 5 μM) induced cytotoxicity. Hypoxic treatment induced the production of peroxynitrite and promoted NSC/INS; proliferation and self-renewal, and neuronal differentiation. Treatments of peroxynitrite decomposition catalysts (PDCs, FeTMPyP and FeTPPS) reduced hypoxia-induced peroxynitrite formation, NSC/INS; proliferation, self-renewal and neuronal differentiation. The neurogenesis promoting effects were partly mediated through activating Wnt/β-catenin signaling pathway. Conclusion: Low concentration of peroxynitrite may serve as a cellular signaling for promoting NSC/INS; proliferation, self-renewal and neuronal differentiation. Copyright © 2013 Published by Elsevier B.V.-
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/jns-
dc.relation.ispartofJournal of the Neurological Sciencesen_US
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in Journal of the Neurological Sciences. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Journal of the Neurological Sciences, 2013, v. 333 n. Suppl. 1, p. e228 DOI# 10.1016/j.jns.2013.07.896-
dc.titlePeroxynitrite could regulate proliferation and neuronal differentiation of neural stem/progenitor cells through activating WNT/β-catenin signaling pathwayen_US
dc.typeConference_Paperen_US
dc.identifier.emailShen, J: shenjg@hku.hken_US
dc.identifier.emailChen, XM: chenxm@hku.hk-
dc.identifier.authorityShen, J=rp00487en_US
dc.identifier.doi10.1016/j.jns.2013.07.896-
dc.identifier.hkuros233604en_US
dc.identifier.volume333-
dc.identifier.issueSuppl. 1-
dc.identifier.spagee228-
dc.identifier.epagee228-
dc.publisher.placeNetherlands-

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