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Article: Bone morphogenetic proteins mediate cellular response and, together with Noggin, regulate astrocyte differentiation after spinal cord injury

TitleBone morphogenetic proteins mediate cellular response and, together with Noggin, regulate astrocyte differentiation after spinal cord injury
Authors
Issue Date2010
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexnr
Citation
Experimental Neurology, 2010, v. 221 n. 2, p. 353-366 How to Cite?
AbstractBone morphogenetic proteins (BMPs) play a critical role in regulating cell fate determination during central nervous system (CNS) development. In light of recent findings that BMP-2/4/7 expressions are upregulated after spinal cord injury, we hypothesized that the BMP signaling pathway is important in regulating cellular composition in the injured spinal cord. We found that BMP expressions were upregulated in neural stem cells (NSCs), neurons, oligodendrocytes and microglia/macrophages. Increased expression levels of pSmad1/5/8 (downstream molecules of BMP) were detected in neurons, NSCs, astrocytes, oligodendrocytes and oligodendroglial progenitor cells (OPCs). Active astrocytes which form the astroglial scar were probably derived from NSCs, OPCs and resident astrocytes. Since quiescent NSCs in the normal adult spinal cord will proliferate and differentiate actively into neural cells after traumatic injury, we proposed that BMPs can regulate cellular components by controlling NSC differentiation. Neurosphere culture from adult mouse spinal cord showed that BMP-4 promoted astrocyte differentiation from NSCs while suppressing production of neurons and oligodendrocytes. Conversely, inhibition of BMP-4 by Noggin notably decreased the ratio of astrocyte to neuron numbers. However, intrathecal administration of Noggin in the injured spinal cord failed to attenuate glial fibrillar acidic protein (GFAP) expression even though it effectively reduced pSmad expression. Noggin treatment did not block phosphorylation of Stat3 and the induction of GFAP in the injured spinal cord, suggesting that in addition to the BMP/Smad pathway, the JAK/STAT pathway may also be involved in the regulation of GFAP expression after spinal cord injury. © 2009 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/124470
ISSN
2015 Impact Factor: 4.657
2015 SCImago Journal Rankings: 2.427
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXiao, Qen_HK
dc.contributor.authorDu, Yen_HK
dc.contributor.authorWu, Wen_HK
dc.contributor.authorYip, HKen_HK
dc.date.accessioned2010-10-31T10:36:12Z-
dc.date.available2010-10-31T10:36:12Z-
dc.date.issued2010en_HK
dc.identifier.citationExperimental Neurology, 2010, v. 221 n. 2, p. 353-366en_HK
dc.identifier.issn0014-4886en_HK
dc.identifier.urihttp://hdl.handle.net/10722/124470-
dc.description.abstractBone morphogenetic proteins (BMPs) play a critical role in regulating cell fate determination during central nervous system (CNS) development. In light of recent findings that BMP-2/4/7 expressions are upregulated after spinal cord injury, we hypothesized that the BMP signaling pathway is important in regulating cellular composition in the injured spinal cord. We found that BMP expressions were upregulated in neural stem cells (NSCs), neurons, oligodendrocytes and microglia/macrophages. Increased expression levels of pSmad1/5/8 (downstream molecules of BMP) were detected in neurons, NSCs, astrocytes, oligodendrocytes and oligodendroglial progenitor cells (OPCs). Active astrocytes which form the astroglial scar were probably derived from NSCs, OPCs and resident astrocytes. Since quiescent NSCs in the normal adult spinal cord will proliferate and differentiate actively into neural cells after traumatic injury, we proposed that BMPs can regulate cellular components by controlling NSC differentiation. Neurosphere culture from adult mouse spinal cord showed that BMP-4 promoted astrocyte differentiation from NSCs while suppressing production of neurons and oligodendrocytes. Conversely, inhibition of BMP-4 by Noggin notably decreased the ratio of astrocyte to neuron numbers. However, intrathecal administration of Noggin in the injured spinal cord failed to attenuate glial fibrillar acidic protein (GFAP) expression even though it effectively reduced pSmad expression. Noggin treatment did not block phosphorylation of Stat3 and the induction of GFAP in the injured spinal cord, suggesting that in addition to the BMP/Smad pathway, the JAK/STAT pathway may also be involved in the regulation of GFAP expression after spinal cord injury. © 2009 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexnren_HK
dc.relation.ispartofExperimental Neurologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAstrocytes - drug effectsen_HK
dc.subject.meshBone Morphogenetic Proteins - pharmacology - therapeutic useen_HK
dc.subject.meshBromodeoxyuridine - metabolismen_HK
dc.subject.meshCarrier Proteins - pharmacology - therapeutic useen_HK
dc.subject.meshCell Differentiation - drug effectsen_HK
dc.subject.meshCell Proliferation - drug effectsen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshDisease Models, Animalen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Regulation - drug effectsen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshMyelin Basic Proteins - genetics - metabolismen_HK
dc.subject.meshNerve Tissue Proteins - genetics - metabolismen_HK
dc.subject.meshNeuronsen_HK
dc.subject.meshNuclear Proteins - genetics - metabolismen_HK
dc.subject.meshOligodendroglia - drug effectsen_HK
dc.subject.meshRNA, Messenger - metabolismen_HK
dc.subject.meshSignal Transduction - drug effects - physiologyen_HK
dc.subject.meshSpinal Cord Injuries - drug therapy - pathology - physiopathologyen_HK
dc.subject.meshStem Cells - drug effectsen_HK
dc.subject.meshTime Factorsen_HK
dc.titleBone morphogenetic proteins mediate cellular response and, together with Noggin, regulate astrocyte differentiation after spinal cord injuryen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0014-4886&volume=221&spage=353&epage=366&date=2010&atitle=Bone+Morphogenetic+Proteins+Mediate+Cellular+Response+And,+Together+With+Noggin,+Regulate+Astrocyte+Differentiation+After+Spinal+Cord+Injuryen_HK
dc.identifier.emailWu, W:wtwu@hkucc.hku.hken_HK
dc.identifier.emailYip, HK:hkfyip@hku.hken_HK
dc.identifier.authorityWu, W=rp00419en_HK
dc.identifier.authorityYip, HK=rp00285en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.expneurol.2009.12.003en_HK
dc.identifier.pmid20005873-
dc.identifier.scopuseid_2-s2.0-73949095800en_HK
dc.identifier.hkuros176339en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-73949095800&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume221en_HK
dc.identifier.issue2en_HK
dc.identifier.spage353en_HK
dc.identifier.epage366en_HK
dc.identifier.eissn1090-2430-
dc.identifier.isiWOS:000274560800010-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXiao, Q=35621162200en_HK
dc.identifier.scopusauthoridDu, Y=36993717500en_HK
dc.identifier.scopusauthoridWu, W=7407081122en_HK
dc.identifier.scopusauthoridYip, HK=7101980864en_HK
dc.identifier.citeulike6407666-

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