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Article: MiR-637 maintains the balance between adipocytes and osteoblasts by directly targeting Osterix

TitleMiR-637 maintains the balance between adipocytes and osteoblasts by directly targeting Osterix
Authors
Issue Date2011
PublisherAmerican Society for Cell Biology. The Journal's web site is located at http://www.molbiolcell.org/
Citation
Molecular Biology Of The Cell, 2011, v. 22 n. 21, p. 3955-3961 How to Cite?
AbstractBone development is dynamically regulated by homeostasis, in which a balance between adipocytes and osteoblasts is maintained. Disruption of this differentiation balance leads to various bone-related metabolic diseases, including osteoporosis. In the present study, a primate-specific microRNA (miR-637) was found to be involved in the differentiation of human mesenchymal stem cells (hMSCs). Our preliminary data indicated that miR-637 suppressed the growth of hMSCs and induced S-phase arrest. Expression of miR-637 was increased during adipocyte differentiation (AD), whereas it was decreased during osteoblast differentiation (OS), which suggests miR-637 could act as a mediator of adipoosteogenic differentiation. Osterix (Osx), a significant transcription factor of osteoblasts, was shown to be a direct target of miR-637, which significantly enhanced AD and suppressed OS in hMSCs through direct suppression of Osx expression. Furthermore, miR-637 also significantly enhanced de novo adipogenesis in nude mice. In conclusion, our data indicated that the expression of miR-637 was indispensable for maintaining the balance of adipocytes and osteoblasts. Disruption of miR-637 expression patterns leads to irreversible damage to the balance of differentiation in bone marrow. © 2011 Zhang et al.
Persistent Identifierhttp://hdl.handle.net/10722/168582
ISSN
2015 Impact Factor: 4.037
2015 SCImago Journal Rankings: 3.665
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, JFen_US
dc.contributor.authorFu, WMen_US
dc.contributor.authorHe, MLen_US
dc.contributor.authorWang, Hen_US
dc.contributor.authorWang, WMen_US
dc.contributor.authorYu, SCen_US
dc.contributor.authorBian, XWen_US
dc.contributor.authorZhou, Jen_US
dc.contributor.authorLin, MCMen_US
dc.contributor.authorLu, Gen_US
dc.contributor.authorPoon, WSen_US
dc.contributor.authorKung, HFen_US
dc.date.accessioned2012-10-08T03:21:05Z-
dc.date.available2012-10-08T03:21:05Z-
dc.date.issued2011en_US
dc.identifier.citationMolecular Biology Of The Cell, 2011, v. 22 n. 21, p. 3955-3961en_US
dc.identifier.issn1059-1524en_US
dc.identifier.urihttp://hdl.handle.net/10722/168582-
dc.description.abstractBone development is dynamically regulated by homeostasis, in which a balance between adipocytes and osteoblasts is maintained. Disruption of this differentiation balance leads to various bone-related metabolic diseases, including osteoporosis. In the present study, a primate-specific microRNA (miR-637) was found to be involved in the differentiation of human mesenchymal stem cells (hMSCs). Our preliminary data indicated that miR-637 suppressed the growth of hMSCs and induced S-phase arrest. Expression of miR-637 was increased during adipocyte differentiation (AD), whereas it was decreased during osteoblast differentiation (OS), which suggests miR-637 could act as a mediator of adipoosteogenic differentiation. Osterix (Osx), a significant transcription factor of osteoblasts, was shown to be a direct target of miR-637, which significantly enhanced AD and suppressed OS in hMSCs through direct suppression of Osx expression. Furthermore, miR-637 also significantly enhanced de novo adipogenesis in nude mice. In conclusion, our data indicated that the expression of miR-637 was indispensable for maintaining the balance of adipocytes and osteoblasts. Disruption of miR-637 expression patterns leads to irreversible damage to the balance of differentiation in bone marrow. © 2011 Zhang et al.en_US
dc.languageengen_US
dc.publisherAmerican Society for Cell Biology. The Journal's web site is located at http://www.molbiolcell.org/en_US
dc.relation.ispartofMolecular Biology of the Cellen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshAdipocytes - Metabolism - Physiologyen_US
dc.subject.meshAdipogenesis - Geneticsen_US
dc.subject.meshAdipose Tissue - Anatomy & Histology - Physiologyen_US
dc.subject.meshAdulten_US
dc.subject.meshAlkaline Phosphatase - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Cycle Checkpointsen_US
dc.subject.meshCell Proliferationen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshEnzyme Assaysen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expressionen_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshHumansen_US
dc.subject.meshMesenchymal Stem Cellsen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Nudeen_US
dc.subject.meshMicrornas - Genetics - Metabolismen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshOsteoblasts - Metabolism - Physiologyen_US
dc.subject.meshTranscription Factors - Genetics - Metabolismen_US
dc.titleMiR-637 maintains the balance between adipocytes and osteoblasts by directly targeting Osterixen_US
dc.typeArticleen_US
dc.identifier.emailLin, MCM:mcllin@hkucc.hku.hken_US
dc.identifier.authorityLin, MCM=rp00746en_US
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1091/mbc.E11-04-0356en_US
dc.identifier.pmid21880893-
dc.identifier.pmcidPMC3204058-
dc.identifier.scopuseid_2-s2.0-80655125005en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80655125005&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume22en_US
dc.identifier.issue21en_US
dc.identifier.spage3955en_US
dc.identifier.epage3961en_US
dc.identifier.isiWOS:000296603300012-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridZhang, JF=13007942600en_US
dc.identifier.scopusauthoridFu, WM=52463551200en_US
dc.identifier.scopusauthoridHe, ML=35080389700en_US
dc.identifier.scopusauthoridWang, H=8748902500en_US
dc.identifier.scopusauthoridWang, WM=54409697600en_US
dc.identifier.scopusauthoridYu, SC=25629204700en_US
dc.identifier.scopusauthoridBian, XW=7103023096en_US
dc.identifier.scopusauthoridZhou, J=7405550537en_US
dc.identifier.scopusauthoridLin, MCM=7404816359en_US
dc.identifier.scopusauthoridLu, G=36619108300en_US
dc.identifier.scopusauthoridPoon, WS=7103025507en_US
dc.identifier.scopusauthoridKung, HF=7402514190en_US

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