Aging-dependent regulatory cells emerge in subcutaneous fat to inhibit adipogenesis.
Aging-dependent regulatory cells emerge in subcutaneous fat to inhibit adipogenesis.
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DOI：
10.1016/j.devcel.2021.03.026
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发表时间：
2021-05-17
影响因子：
11.8
通讯作者：
Sul HS
中科院分区：
文献类型：
--
作者：
Nguyen HP;Lin F;Yi D;Xie Y;Dinh J;Xue P;Sul HS
脂肪组织质量和肥胖在整个生命周期中都会发生变化。在衰老过程中，虽然内脏脂肪组织（VAT）趋于增加，但外周皮下脂肪组织（SAT）显著减少。与VAT不同，VAT与代谢疾病有关，包括2型糖尿病，SAT具有有益的效果。然而，衰老相关的SAT丢失背后的分子细节仍不清楚。在这里，通过比较来自年轻和老龄小鼠的SAT的总基质血管细胞的scRNA-seq，我们鉴定了仅在老龄小鼠和人类的SAT中出现的衰老依赖性调节细胞（ARC）群体。ARC表达脂肪祖细胞标志物，但缺乏脂肪形成能力;它们分泌高水平的促炎趋化因子，包括Ccl 6，以抑制邻近脂肪前体的增殖和分化。我们还发现Pu.1是ARC发展的驱动因素。我们确定了一个ARC人口和它的能力，以抑制分化的邻近脂肪前体，与衰老相关的损失SAT。Nguyen等人鉴定了衰老过程中在皮下脂肪组织（SAT）中特异性出现的衰老依赖性调节细胞（ARC）群体。ARC抑制邻近成脂前体的分化和增殖，并可能导致衰老过程中SAT的丧失。Pu.1对ARC的发育和表型至关重要。
Adipose tissue mass and adiposity change throughout the lifespan. During aging, while visceral adipose tissue (VAT) tends to increase, peripheral subcutaneous adipose tissue (SAT) decreases significantly. Unlike VAT, which is linked to metabolic diseases, including type 2 diabetes, SAT has beneficial effects. However, the molecular details behind the aging-associated loss of SAT remain unclear. Here, by comparing scRNA-seq of total stromal vascular cells of SAT from young and aging mice, we identify an Aging-dependent Regulatory Cell (ARC) population that emerges only in SAT of aged mice and humans. ARC express adipose progenitor markers but lacks adipogenic capacity; they secrete high levels of pro-inflammatory chemokines, including Ccl6, to inhibit proliferation and differentiation of neighboring adipose precursors. We also found Pu.1 to be a driving factor for ARC development. We identify an ARC population and its capacity to inhibit differentiation of neighboring adipose precursors, correlating with aging-associated loss of SAT. Nguyen et al. identify an Aging-dependent Regulatory Cell (ARC) population that emerges specifically in subcutaneous adipose tissue (SAT) during aging. ARCs inhibit differentiation and proliferation of neighboring adipogenic precursors and may contribute to loss of SAT during aging. Pu.1 is critical for ARC development and phenotype of ARC.
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影响因子：
5.2
作者：
Hudak CS;Sul HS
通讯作者：
Sul HS
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通讯作者：
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影响因子：
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通讯作者：
Casteilla, L.
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影响因子：
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作者：
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通讯作者：
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