Please use this identifier to cite or link to this item:
http://hdl.handle.net/1843/53891
Full metadata record
DC Field | Value | Language |
---|---|---|
dc.creator | Geneviève Marcelin | pt_BR |
dc.creator | Adaliene Versiani Matos Ferreira | pt_BR |
dc.creator | Yuejun Liu | pt_BR |
dc.creator | Michael Atlan | pt_BR |
dc.creator | Judith Aron-Wisnewsky | pt_BR |
dc.creator | Véronique Pelloux | pt_BR |
dc.creator | Yair Botbol | pt_BR |
dc.creator | Marc Ambrosini | pt_BR |
dc.creator | Magali Fradet | pt_BR |
dc.creator | Christine Rouault | pt_BR |
dc.creator | Corneliu Hénégar | pt_BR |
dc.creator | Jean-Sébastien Hulot | pt_BR |
dc.creator | Christine Poitou | pt_BR |
dc.creator | Adriana Torcivia | pt_BR |
dc.creator | Raphael Nail-Barthelemy | pt_BR |
dc.creator | Jean-Christophe Bichet | pt_BR |
dc.creator | Emmanuel L. Gautier | pt_BR |
dc.creator | Karine Clément | pt_BR |
dc.date.accessioned | 2023-05-24T19:37:06Z | - |
dc.date.available | 2023-05-24T19:37:06Z | - |
dc.date.issued | 2017 | - |
dc.citation.volume | 25 | pt_BR |
dc.citation.issue | 3 | pt_BR |
dc.citation.spage | 673 | pt_BR |
dc.citation.epage | 685 | pt_BR |
dc.identifier.doi | https://doi.org/10.1016/j.cmet.2017.01.010 | pt_BR |
dc.identifier.issn | 1932-7420 | pt_BR |
dc.identifier.uri | http://hdl.handle.net/1843/53891 | - |
dc.description.resumo | Obesity-induced white adipose tissue (WAT) fibrosis is believed to accelerate WAT dysfunction. However, the cellular origin of WAT fibrosis remains unclear. Here, we show that adipocyte platelet-derived growth factor receptor-a-positive (PDGFRa+) progenitors adopt a fibrogenic phenotype in obese mice prone to visceral WAT fibrosis. More specifically, a subset of PDGFRa+ cells with high CD9 expression (CD9high) originates pro-fibrotic cells whereas their CD9low counterparts, committed to adipogenesis, are almost completely lost in the fibrotic WAT. PDGFRa pathway activation promotes a phenotypic shift toward PDGFRa+ CD9high fibrogenic cells, driving pathological remodeling and altering WAT function in obesity. These findings translated to human obesity as the frequency of CD9high progenitors in omental WAT (oWAT) correlates with oWAT fibrosis level, insulin-resistance severity, and type 2 diabetes. Collectively, our data demonstrate that in addition to representing a WAT adipogenic niche, different PDGFRa+ cell subsets modulate obesity-induced WAT fibrogenesis and are associated with loss of metabolic fitness. | pt_BR |
dc.description.sponsorship | CAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superior | pt_BR |
dc.description.sponsorship | Outra Agência | pt_BR |
dc.format.mimetype | pt_BR | |
dc.language | eng | pt_BR |
dc.publisher | Universidade Federal de Minas Gerais | pt_BR |
dc.publisher.country | Brasil | pt_BR |
dc.publisher.department | ENF - DEPARTAMENTO DE NUTRIÇÃO | pt_BR |
dc.publisher.initials | UFMG | pt_BR |
dc.relation.ispartof | Cell Metabolism | pt_BR |
dc.rights | Acesso Aberto | pt_BR |
dc.subject | White adipose tissue | pt_BR |
dc.subject | Obesity | pt_BR |
dc.subject | Fibrosis | pt_BR |
dc.subject.other | Tecido adiposo branco | pt_BR |
dc.subject.other | Obesidade | pt_BR |
dc.subject.other | Fibrose | pt_BR |
dc.title | A PDGFRα-Mediated switch toward CD9ʰᶦᵍʰ adipocyte progenitors controls obesity-induced adipose tissue fibrosis | pt_BR |
dc.type | Artigo de Periódico | pt_BR |
dc.url.externa | https://www.sciencedirect.com/science/article/pii/S1550413117300451?via%3Dihub | pt_BR |
dc.identifier.orcid | https://orcid.org/0000-0002-9779-5529 | pt_BR |
dc.identifier.orcid | https://orcid.org/0000-0003-2256-8652 | pt_BR |
dc.identifier.orcid | https://orcid.org/0000-0002-8486-5591 | pt_BR |
dc.identifier.orcid | https://orcid.org/0000-0001-5463-6117 | pt_BR |
dc.identifier.orcid | https://orcid.org/0000-0003-2976-7566 | pt_BR |
Appears in Collections: | Artigo de Periódico |
Files in This Item:
File | Description | Size | Format | |
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A PDGFRα-Mediated Switch toward CD9high Adipocyte Progenitors Controls Obesity-Induced Adipose Tissue Fibrosis.pdf | 3.04 MB | Adobe PDF | View/Open |
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