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首页> 外文期刊>Cell metabolism >A PDGFR alpha-Mediated Switch toward CD9(high) Adipocyte Progenitors Controls Obesity-Induced Adipose Tissue Fibrosis
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A PDGFR alpha-Mediated Switch toward CD9(high) Adipocyte Progenitors Controls Obesity-Induced Adipose Tissue Fibrosis

机译：PDGFRα-介导的开关朝CD9（高）adipocyte祖细胞控制肥胖诱导的脂肪组织纤维化

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摘要

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-alpha-positive (PDGFR alpha(+)) progenitors adopt a fibrogenic phenotype in obese mice prone to visceral WAT fibrosis. More specifically, a subset of PDGFR alpha(+) cells with high CD9 expression (CD9(high)) originates pro-fibrotic cells whereas their CD9(low) counterparts, committed to adipogenesis, are almost completely lost in the fibrotic WAT. PDGFRa pathway activation promotes a phenotypic shift toward PDGFR alpha(+) CD9(high) fibrogenic cells, driving pathological remodeling and altering WAT function in obesity. These findings translated to human obesity as the frequency of CD9(high) 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 PDGFR alpha(+) cell subsets modulate obesity-induced WAT fibrogenesis and are associated with loss of metabolic fitness.
机译：肥胖诱导的白色脂肪组织（WAT）纤维化被认为会加速WAT功能障碍。然而，WAT纤维化的细胞起源尚不清楚。在这里，我们发现脂肪细胞血小板衍生生长因子受体α阳性（PDGFRα（+））祖细胞在易发生内脏WAT纤维化的肥胖小鼠中具有纤维化表型。更具体地说，具有高CD9表达（CD9（高））的PDGFRα（+）细胞的一个子集起源于促纤维化细胞，而其致力于脂肪生成的CD9（低）对应物在纤维化细胞中几乎完全丢失。PDGFRa通路激活促进表型向PDGFRα（+）CD9（高）成纤维细胞转变，在肥胖中驱动病理重塑并改变WAT功能。这些发现转化为人类肥胖，因为大网膜WAT（oWAT）中CD9（高）祖细胞的频率与oWAT纤维化水平、胰岛素抵抗严重程度和2型糖尿病相关。总的来说，我们的数据表明，除了代表WAT脂肪生成生态位外，不同的PDGFRα（+）细胞亚群调节肥胖诱导的WAT纤维生成，并与代谢适应性的丧失有关。

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