p53 Induces skin aging by depleting Blimp1+ sebaceous gland cells.
p53 Induces skin aging by depleting Blimp1+ sebaceous gland cells.
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DOI：
10.1038/cddis.2014.87
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发表时间：
2014-03-27
影响因子：
9
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中科院分区：
文献类型：
--
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p53是机体衰老的重要诱导剂。然而，其在皮肤老化中的作用仍不清楚。在这里，我们发现，p53 慢性激活的小鼠皮肤会出现与皮下脂肪减少和皮脂腺 (SG) 减少相关的衰老表型。脂肪层的减少可能是由于哺乳动物 TOR 复合物 1 (mTORC1) 活性的降低，伴随着能量消耗基因表达的升高，并且可能作为补偿效应，导致过氧化物酶体增殖物激活受体 (PPAR)γ（皮脂细胞分化的诱导剂）的升高。此外，Blimp1+ 皮脂细胞随着细胞衰老的增加而耗尽，这可以通过 PPARγ 拮抗剂 (BADGE) 治疗来逆转。因此，我们的结果表明，p53 介导的皮肤衰老不仅涉及皮下脂肪减少导致的皮肤变薄，还涉及皮脂腺活性下降导致的皮肤干燥或干燥。
p53 is an important inducer of organismal aging. However, its roles in the aging of skin remain unclear. Here we show that mice with chronic activation of p53 develop an aging phenotype in the skin associated with a reduction of subcutaneous fat and loss of sebaceous gland (SG). The reduction in the fat layer may result from the decrease of mammalian TOR complex 1 (mTORC1) activity accompanied by elevated expression of energy expenditure genes, and possibly as compensatory effects, leading to the elevation of peroxisome proliferator-activated receptor (PPAR)γ, an inducer of sebocyte differentiation. In addition, Blimp1+ sebocytes become depleted concomitantly with an increase in cellular senescence, which can be reversed by PPARγ antagonist (BADGE) treatment. Therefore, our results indicate that p53-mediated aging of the skin involves not only thinning through the loss of subdermal fat, but also xerosis or drying of the skin through declining sebaceous gland activity.
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