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dc.contributor.authorSecco, Blandine
dc.contributor.authorLee, Peter L.
dc.contributor.authorGuertin, David A.
dc.contributor.authorLaplante, Mathieu
dc.date2022-08-11T08:09:21.000
dc.date.accessioned2022-08-23T16:27:11Z
dc.date.available2022-08-23T16:27:11Z
dc.date.issued2017-01-03
dc.date.submitted2017-05-25
dc.identifier.citationCell Rep. 2017 Jan 3;18(1):93-106. doi: 10.1016/j.celrep.2016.12.015. <a href="https://doi.org/10.1016/j.celrep.2016.12.015">Link to article on publisher's site</a>
dc.identifier.issn2211-1247 (Electronic)
dc.identifier.doi10.1016/j.celrep.2016.12.015
dc.identifier.pmid28052263
dc.identifier.urihttp://hdl.handle.net/20.500.14038/36726
dc.description<p>Full author list omitted for brevity. For the full list of authors, see article.</p>
dc.description.abstractDespite progress in our comprehension of the mechanisms regulating adipose tissue development, the nature of the factors that functionally characterize adipose precursors is still elusive. Defining the early steps regulating adipocyte development is needed for the generation of tools to control adipose tissue size and function. Here, we report the discovery of V-set and transmembrane domain containing 2A (VSTM2A) as a protein expressed and secreted by committed preadipocytes. VSTM2A expression is elevated in the early phases of adipogenesis in vitro and adipose tissue development in vivo. We show that VSTM2A-producing cells associate with the vasculature and express the common surface markers of adipocyte progenitors. Overexpression of VSTM2A induces adipogenesis, whereas its depletion impairs this process. VSTM2A controls preadipocyte determination at least in part by modulating BMP signaling and PPARgamma2 activation. We propose a model in which VSTM2A is produced to preserve and amplify the adipogenic capability of adipose precursors.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=28052263&dopt=Abstract">Link to Article in PubMed</a>
dc.rightsCopyright 2017 The Author(s).
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject3T3-L1
dc.subjectadipogenesis
dc.subjectadipogenic commitment
dc.subjectadipose tissue
dc.subjectcell differentiation
dc.subjectcell signaling
dc.subjectobesity
dc.subjectpreadipocyte
dc.subjectBiochemistry
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectDevelopmental Biology
dc.subjectMolecular Biology
dc.titleAmplification of Adipogenic Commitment by VSTM2A
dc.typeJournal Article
dc.source.journaltitleCell reports
dc.source.volume18
dc.source.issue1
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1092&amp;context=metnet_pubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/metnet_pubs/93
dc.identifier.contextkey10212158
refterms.dateFOA2022-08-23T16:27:11Z
html.description.abstract<p>Despite progress in our comprehension of the mechanisms regulating adipose tissue development, the nature of the factors that functionally characterize adipose precursors is still elusive. Defining the early steps regulating adipocyte development is needed for the generation of tools to control adipose tissue size and function. Here, we report the discovery of V-set and transmembrane domain containing 2A (VSTM2A) as a protein expressed and secreted by committed preadipocytes. VSTM2A expression is elevated in the early phases of adipogenesis in vitro and adipose tissue development in vivo. We show that VSTM2A-producing cells associate with the vasculature and express the common surface markers of adipocyte progenitors. Overexpression of VSTM2A induces adipogenesis, whereas its depletion impairs this process. VSTM2A controls preadipocyte determination at least in part by modulating BMP signaling and PPARgamma2 activation. We propose a model in which VSTM2A is produced to preserve and amplify the adipogenic capability of adipose precursors.</p>
dc.identifier.submissionpathmetnet_pubs/93
dc.contributor.departmentUMass Metabolic Network
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages93-106


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Copyright 2017 The Author(s).
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