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Aging Cell:抑制长寿基因SIRT2可治疗神经病变

2021-06-04 haibei MedSci原创

最近,研究人员发文报告了野生型GARS与NAD+依赖性去乙酰化酶SIRT2结合并抑制其去乙酰化活性,导致α-微管蛋白乙酰化。

Charcot-Marie-Tooth病是一种最常见的遗传性周围神经肌肉疾病,每2500人中就有一人受到影响。甘氨酰-tRNA合成酶(GARS)基因的显性突变可以引起周围神经变性,导致CMT疾病2D型。至今为止,GARS(GARSCMT2D)的突变在疾病发病机制中的潜在机制还没有被完全理解。

已有的研究表明。周围轴突需要一个组织良好的微管网络,以便有效地在体细胞和突触之间运输囊泡。微管内α-微管蛋白的乙酰化促进了分子马达驱动蛋白的锚定并刺激了囊泡的运输。此外,乙酰化的微管比非乙酰化的微管更稳定,对药物引起的解聚更有抵抗力。轴突运输的缺陷往往与神经变性有关,特别是与周围神经病有关。

SIRT2属于第三类组蛋白去乙酰化酶,控制几种蛋白质的乙酰化状态,包括α-微管蛋白。靶向SIRT2的活性对帕金森病(PD)和亨廷顿病(HD)有益,但对CMT无益。有两项研究报告称,针对α-微管蛋白的另一种去乙酰化酶HDAC6可能对GARS诱导的CMT疾病有潜在的治疗作用。

虽然SIRT2可以在体外使α-微管蛋白去乙酰化,但在小鼠中敲除SIRT2并不改变体内α-微管蛋白的乙酰化水平,表明SIRT2可能在特殊条件下使α-微管蛋白去乙酰化。例如,SIRT2,而不是HDAC6,负责小鼠巨噬细胞炎症体激活期间α-微管蛋白的去乙酰化。

最近,研究人员发文报告了野生型GARS与NAD+依赖性去乙酰化酶SIRT2结合并抑制其去乙酰化活性,导致α-微管蛋白乙酰化,这是SIRT2的主要底物。GARS的催化结构域与SIRT2紧密相互作用,这正好也是CMT2D突变的定位

SIRT2敲降可以挽救CMT相关表型和果蝇寿命。

然而,CMT2D突变的GARS不能抑制SIRT2的去乙酰化,从而导致乙酰化α-微管蛋白的减少。果蝇模型中SIRT2的遗传性抑制可以挽救GARS引起的轴突性CMT神经病变,并延长寿命

因此,该研究结果证明了SIRT2依赖的α-微管蛋白去乙酰化在突变体GARS诱导的神经系统疾病中的致病作用,并为靶向SIRT2作为对抗遗传性轴突病的潜在疗法提供了新的视角。

 

原始出处:

Yingying Zhao et al. SIRT2-knockdown rescues GARS-induced Charcot-Marie-Tooth neuropathy. Aging Cell (2021). 

 

 

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    2021-06-10 维他命
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    2021-06-06 axin012
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