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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Deletion of Nrip1 Extends Female Mice Longevity, Increases Autophagy, and Delays Cell Senescence
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Deletion of Nrip1 Extends Female Mice Longevity, Increases Autophagy, and Delays Cell Senescence

机译：缺失NRIP1延长了女性小鼠寿命，增加自噬，延迟细胞衰老

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Using age of female sexual maturation as a biomarker, we previously identified nuclear receptor interacting protein 1 (Nrip1) as a candidate gene that may regulate aging and longevity. In the current report, we found that the deletion of Nrip1 can significantly extend longevity of female mice (log-rank test, p = .0004). We also found that Nrip1 expression is altered differently in various tissues during aging and under diet restriction. Remarkably, Nrip1 expression is elevated with aging in visceral white adipose tissue (WAT), but significantly reduced after 4 months of diet restriction. However, in gastrocnemius muscle, Nrip1 expression is significantly upregulated after the diet restriction. In mouse embryonic fibroblasts, we found that the deletion of Nrip1 can suppress fibroblast proliferation, enhance autophagy under normal culture or amino acid starvation conditions, as well as delay oxidative and replicative senescence. Importantly, in WAT of old animals, the deletion of the Nrip could significantly upregulate autophagy and reduce the number of senescent cells. These results suggest that deleting Nrip1 can extend female longevity, but tissue-specific deletion may have varying effects on health span. The deletion of Nrip1 in WAT may delay senescence in WAT and extend health span.
机译：利用女性性成熟年龄作为生物标志物，我们之前确定核受体相互作用蛋白1（Nrip1）是可能调节衰老和寿命的候选基因。在目前的报告中，我们发现删除Nrip1可以显著延长雌性小鼠的寿命（对数秩检验，p=0.0004）。我们还发现，Nrip1的表达在衰老和饮食限制下的不同组织中发生了不同的变化。值得注意的是，Nrip1在内脏白色脂肪组织（WAT）中的表达随着年龄的增长而升高，但在限制饮食4个月后显著降低。然而，在腓肠肌中，Nrip1的表达在饮食限制后显著上调。在小鼠胚胎成纤维细胞中，我们发现Nrip1的缺失可以抑制成纤维细胞增殖，在正常培养或氨基酸饥饿条件下增强自噬，以及延迟氧化和复制性衰老。重要的是，在老年动物的WAT中，Nrip的缺失可以显著上调自噬并减少衰老细胞的数量。这些结果表明，删除Nrip1可以延长女性寿命，但组织特异性删除可能会对健康跨度产生不同的影响。WAT中Nrip1的缺失可能延缓WAT的衰老，延长健康寿命。

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