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Article: Sur8/Shoc2 involves both inhibition of differentiation and maintenance of self-renewal of neural progenitor cells via modulation of extracellular signal-regulated kinase signaling

TitleSur8/Shoc2 involves both inhibition of differentiation and maintenance of self-renewal of neural progenitor cells via modulation of extracellular signal-regulated kinase signaling
Authors
Issue Date2011
PublisherAlphaMed Press, Inc. The Journal's web site is located at http://www.stemcells.com
Citation
Stem Cells, 2011, v. 29 n. 2, p. 320-331 How to Cite?
AbstractSur8/Shoc2 is a scaffold protein that regulates the Rasextracellular signal-regulated kinase (ERK) pathway. However, the roles of Sur8 in cellular physiologies are poorly understood. In this study, Sur8 was severely repressed in the course of neural progenitor cell (NPC) differentiation in the cerebral cortex of developing rat embryos. Similarly, Sur8 was also critically reduced in cultured NPCs, which were induced differentiation by removal of basic fibroblast growth factor (bFGF). Sur8 regulation occurs at the protein level rather than at the mRNA level as revealed by both in situ hybridization and reverse transcriptase polymerase chain reaction analyses. The role of Sur8 in NPC differentiation was confirmed by lentivirus-mediated Sur8 knockdown, which resulted in increased differentiation, whereas exogenous expression of Sur8 inhibited differentiation. Contrastingly, NPC proliferation was promoted by overexpression, but was suppressed by Sur8 knockdown. The role of Sur8 as an antidifferentiation factor in the developing rat brain was confirmed by an ex vivo embryo culture system combined with the lentivirus-mediated Sur8 knockdown. The numbers and sizes of neurospheres were reduced, but neuronal outgrowth was enhanced by the Sur8 knockdown. The Ras-ERK pathway is involved in Sur8-mediated regulations of differentiation, as the treatment of ERK kinase (MEK) inhibitors blocks the effects of Sur8. The regulations of NPCs' differentiation and proliferation by the Ras-ERK pathway were also shown by the rescues of the effects of bFGF depletion, neuronal differentiation, and antiproliferation by epidermal growth factor. In summary, Sur8 is an antidifferentiation factor that stimulates proliferation for maintenance of self-renewal in NPCs via modulation of the Ras-ERK pathway. © AlphaMed Press.
Persistent Identifierhttp://hdl.handle.net/10722/169576
ISSN
2015 Impact Factor: 5.902
2015 SCImago Journal Rankings: 3.438
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMoon, BSen_US
dc.contributor.authorKim, HYen_US
dc.contributor.authorKim, MYen_US
dc.contributor.authorYang, DHen_US
dc.contributor.authorLee, JMen_US
dc.contributor.authorCho, KWen_US
dc.contributor.authorJung, HSen_US
dc.contributor.authorChoi, KYen_US
dc.date.accessioned2012-10-25T04:53:02Z-
dc.date.available2012-10-25T04:53:02Z-
dc.date.issued2011en_US
dc.identifier.citationStem Cells, 2011, v. 29 n. 2, p. 320-331en_US
dc.identifier.issn1066-5099en_US
dc.identifier.urihttp://hdl.handle.net/10722/169576-
dc.description.abstractSur8/Shoc2 is a scaffold protein that regulates the Rasextracellular signal-regulated kinase (ERK) pathway. However, the roles of Sur8 in cellular physiologies are poorly understood. In this study, Sur8 was severely repressed in the course of neural progenitor cell (NPC) differentiation in the cerebral cortex of developing rat embryos. Similarly, Sur8 was also critically reduced in cultured NPCs, which were induced differentiation by removal of basic fibroblast growth factor (bFGF). Sur8 regulation occurs at the protein level rather than at the mRNA level as revealed by both in situ hybridization and reverse transcriptase polymerase chain reaction analyses. The role of Sur8 in NPC differentiation was confirmed by lentivirus-mediated Sur8 knockdown, which resulted in increased differentiation, whereas exogenous expression of Sur8 inhibited differentiation. Contrastingly, NPC proliferation was promoted by overexpression, but was suppressed by Sur8 knockdown. The role of Sur8 as an antidifferentiation factor in the developing rat brain was confirmed by an ex vivo embryo culture system combined with the lentivirus-mediated Sur8 knockdown. The numbers and sizes of neurospheres were reduced, but neuronal outgrowth was enhanced by the Sur8 knockdown. The Ras-ERK pathway is involved in Sur8-mediated regulations of differentiation, as the treatment of ERK kinase (MEK) inhibitors blocks the effects of Sur8. The regulations of NPCs' differentiation and proliferation by the Ras-ERK pathway were also shown by the rescues of the effects of bFGF depletion, neuronal differentiation, and antiproliferation by epidermal growth factor. In summary, Sur8 is an antidifferentiation factor that stimulates proliferation for maintenance of self-renewal in NPCs via modulation of the Ras-ERK pathway. © AlphaMed Press.en_US
dc.languageengen_US
dc.publisherAlphaMed Press, Inc. The Journal's web site is located at http://www.stemcells.comen_US
dc.relation.ispartofStem Cellsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBrain - Metabolismen_US
dc.subject.meshCell Differentiationen_US
dc.subject.meshCell Proliferationen_US
dc.subject.meshExtracellular Signal-Regulated Map Kinases - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshFibroblast Growth Factor 2 - Metabolismen_US
dc.subject.meshIntracellular Signaling Peptides And Proteins - Genetics - Immunology - Metabolismen_US
dc.subject.meshLeupeptins - Pharmacologyen_US
dc.subject.meshMap Kinase Signaling Systemen_US
dc.subject.meshNeural Stem Cells - Cytology - Metabolismen_US
dc.subject.meshRna Interferenceen_US
dc.subject.meshRna, Messenger - Biosynthesisen_US
dc.subject.meshRna, Small Interferingen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.titleSur8/Shoc2 involves both inhibition of differentiation and maintenance of self-renewal of neural progenitor cells via modulation of extracellular signal-regulated kinase signalingen_US
dc.typeArticleen_US
dc.identifier.emailJung, HS: hsjung@yuhs.acen_US
dc.identifier.authorityJung, HS=rp01683en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/stem.586en_US
dc.identifier.pmid21732489-
dc.identifier.scopuseid_2-s2.0-79952144213en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79952144213&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume29en_US
dc.identifier.issue2en_US
dc.identifier.spage320en_US
dc.identifier.epage331en_US
dc.identifier.isiWOS:000287698600015-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridMoon, BS=15765545200en_US
dc.identifier.scopusauthoridKim, HY=36013294700en_US
dc.identifier.scopusauthoridKim, MY=36120455500en_US
dc.identifier.scopusauthoridYang, DH=26322858200en_US
dc.identifier.scopusauthoridLee, JM=41361401200en_US
dc.identifier.scopusauthoridCho, KW=7403956665en_US
dc.identifier.scopusauthoridJung, HS=7403030195en_US
dc.identifier.scopusauthoridChoi, KY=7403949379en_US

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