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Conference Paper: Notch signaling mediates the switch to fate commitment of bone marrow-derived Schwann cells

TitleNotch signaling mediates the switch to fate commitment of bone marrow-derived Schwann cells
Authors
Issue Date2012
PublisherHKSN & BPHK.
Citation
The Hong Kong-Taiwan Physiology Symposium 2012 and Joint Scientific Meeting of Hong Kong Society of Neurosciences & The Biophysical Society of Hong Kong, Hong Kong, 14-15 June 2012. In Program Book of the Joint Scientific Meeting, 2012, p. 74, abstract P60 How to Cite?
AbstractOur strategy of deriving fate-committed Schwann cells from bone marrow stromal cells (Shea et.al, 2010) supports that the cell-intrinsic switch to fate commitment depends on developing neurons of sensory ganglia. We therefore hypothesize that neurons recoverable from dorsal root ganglia (DRG, E14/15 rats) are at a stage that provides the juxtacrine/paracrine signals for the switch. Analysis of the DRG neurons found cell surface immunopositivities for DLL1, Jagged1 (ligands of Notch receptor) and Neuregulin-1 type III (ligand of ErbB receptors). While bone marrow-derived Schwann cell-like cells (SCLC) were immunopositive for Notch-1, coculture with DRG neurons resulted in progressive increase in ErbB2/B3 expression as revealed by immunocytochemistry and Western blotting. Following activation of the Notch1 receptor – Western blot revealed elevated level of Notch intracellular domain (NICD) during the switch to fate commitment; the level returned to basal when the bone marrow-derived cells tested true for commitment to the Schwann cell fate and in vitro myelination. Our results indicate that DRG neuron-SCLC interaction accomplishes DLL1/Jagged1 -Notch signaling that mediates SCLC expression of the ErbB receptors for signaling interaction with neuregulin-1 type III of DRG neurons. The findings promise the prospect of abundant fate-committed Schwann cells generated from an autologous source for use in nerve repair and regeneration.
DescriptionPoster Presentation: P60
Persistent Identifierhttp://hdl.handle.net/10722/165082

 

DC FieldValueLanguage
dc.contributor.authorTai, EWYen_US
dc.contributor.authorShea, GKHen_US
dc.contributor.authorTsui, AYPen_US
dc.contributor.authorLeung, KHYen_US
dc.contributor.authorChan, YSen_US
dc.contributor.authorShum, DKYen_US
dc.date.accessioned2012-09-20T08:14:40Z-
dc.date.available2012-09-20T08:14:40Z-
dc.date.issued2012en_US
dc.identifier.citationThe Hong Kong-Taiwan Physiology Symposium 2012 and Joint Scientific Meeting of Hong Kong Society of Neurosciences & The Biophysical Society of Hong Kong, Hong Kong, 14-15 June 2012. In Program Book of the Joint Scientific Meeting, 2012, p. 74, abstract P60en_US
dc.identifier.urihttp://hdl.handle.net/10722/165082-
dc.descriptionPoster Presentation: P60-
dc.description.abstractOur strategy of deriving fate-committed Schwann cells from bone marrow stromal cells (Shea et.al, 2010) supports that the cell-intrinsic switch to fate commitment depends on developing neurons of sensory ganglia. We therefore hypothesize that neurons recoverable from dorsal root ganglia (DRG, E14/15 rats) are at a stage that provides the juxtacrine/paracrine signals for the switch. Analysis of the DRG neurons found cell surface immunopositivities for DLL1, Jagged1 (ligands of Notch receptor) and Neuregulin-1 type III (ligand of ErbB receptors). While bone marrow-derived Schwann cell-like cells (SCLC) were immunopositive for Notch-1, coculture with DRG neurons resulted in progressive increase in ErbB2/B3 expression as revealed by immunocytochemistry and Western blotting. Following activation of the Notch1 receptor – Western blot revealed elevated level of Notch intracellular domain (NICD) during the switch to fate commitment; the level returned to basal when the bone marrow-derived cells tested true for commitment to the Schwann cell fate and in vitro myelination. Our results indicate that DRG neuron-SCLC interaction accomplishes DLL1/Jagged1 -Notch signaling that mediates SCLC expression of the ErbB receptors for signaling interaction with neuregulin-1 type III of DRG neurons. The findings promise the prospect of abundant fate-committed Schwann cells generated from an autologous source for use in nerve repair and regeneration.-
dc.languageengen_US
dc.publisherHKSN & BPHK.-
dc.relation.ispartofProgram Book of the Joint Scientific Meetingen_US
dc.titleNotch signaling mediates the switch to fate commitment of bone marrow-derived Schwann cellsen_US
dc.typeConference_Paperen_US
dc.identifier.emailTai, EWY: evietai@hku.hken_US
dc.identifier.emailShea, GKH: grahams@hku.hken_US
dc.identifier.emailTsui, AYP: h0694071@graduate.hku.hken_US
dc.identifier.emailLeung, KHY: echokath@hku.hken_US
dc.identifier.emailChan, YS: yschan@hku.hk-
dc.identifier.emailShum, DKY: shumdkhk@hkucc.hku.hk-
dc.identifier.authorityChan, YS=rp00318en_US
dc.identifier.authorityShum, DKY=rp00321en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros209430en_US
dc.identifier.spage74-
dc.identifier.epage74-
dc.publisher.placeHong Kong-

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