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Nat Cell Biol:德国学者发现关闭Per2基因有助于长寿

摘要 : 2016年4月18日,国际学术权威刊物自然出版集团旗下子刊《Nature Cell Biology》杂志上在线发表了德国莱布尼茨老龄研究所K. Lenhard Rudolph研究员的一篇研究论文,研究人员通过动物实验发现,关闭一种特定基因有助提高实验鼠的免疫力,从而延长寿命。

 

2016年4月18日,国际学术权威刊物自然出版集团旗下子刊《Nature Cell Biology》杂志上在线发表了德国莱布尼茨老龄研究所K. Lenhard Rudolph研究员的一篇研究论文,研究人员通过动物实验发现,关闭一种特定基因有助提高实验鼠的免疫力,从而延长寿命。

通常,伴随动物年龄增长,造血干细胞的功能会逐渐下降,血液中免疫细胞的数量也会下降,免疫力随之降低。在关闭老年实验鼠的Per2基因后,实验鼠的造血干细胞可以更长久地维持其功能,血液中免疫细胞的数量得以保持稳定。这样,老年实验鼠的免疫力依然较强,更不易受到感染而患病,其平均寿命可延长15%。研究人员表示,这一发现是否同样适用于人类还有待进一步研究。

研究人员还发现,有的人Per2基因会发生突变,这种突变会导致睡眠障碍。有这种基因突变的人晚上很早就会发困,无法熬夜。研究人员下一步将研究这种突变是否有积极的一面,如提高老年人的免疫力。

原文链接:

Per2 induction limits lymphoid-biased haematopoietic stem cells and lymphopoiesis in the context of DNA damage and ageing

原文摘要:

Ageing-associated impairments in haemato-lymphopoiesis are associated with DNA damage accumulation and reduced maintenance of lymphoid-biased (Ly-biased) compared with myeloid-biased (My-biased) haematopoietic stem cells (HSCs). Here, in vivo RNAi screening identifies period circadian clock 2 (Per2) as a critical factor limiting the maintenance of HSCs in response to DNA damage and ageing. Under these conditions, Per2 is activated predominantly in Ly-biased HSCs and stimulates DNA damage signalling and p53-dependent apoptosis in haematopoietic cells. Per2 deletion ameliorates replication stress and DNA damage responses in haematopoietic cells, thereby improving the maintenance of Ly-biased HSCs, lymphopoiesis, and immune function in ageing mice without increasing the accumulation of DNA damage. Per2-deficient mice retain Batf/p53-dependent induction of differentiation of HSCs in response to DNA damage and exhibit an elongated lifespan. Together, these results identify Per2 as a negative regulator of Ly-biased HSCs and immune functions in response to DNA damage and ageing.

来源: Nature Cell Biology 浏览次数:0

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