A PDGFRα-Mediated switch toward CD9ʰᶦᵍʰ adipocyte progenitors controls obesity-induced adipose tissue fibrosis
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Universidade Federal de Minas Gerais
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Artigo de periódico
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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.
Abstract
Assunto
Tecido adiposo branco, Obesidade, Fibrose
Palavras-chave
White adipose tissue, Obesity, Fibrosis
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https://www.sciencedirect.com/science/article/pii/S1550413117300451?via%3Dihub