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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Neuropeptide Y Enhances Progerin Clearance and Ameliorates the Senescent Phenotype of Human Hutchinson-Gilford Progeria Syndrome Cells
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Neuropeptide Y Enhances Progerin Clearance and Ameliorates the Senescent Phenotype of Human Hutchinson-Gilford Progeria Syndrome Cells

机译：Neuropeptide Y增强了Progerin清除，改善了人Hutchinson-Gilford Progeria综合征细胞的衰老表型

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Hutchinson-Gilford progeria syndrome (HGPS, or classical progeria) is a rare genetic disorder, characterized by premature aging, and caused by a de novo point mutation (C608G) within the lamin A/C gene (LMNA), producing an abnormal lamin A protein, termed progerin. Accumulation of progerin causes nuclear abnormalities and cell cycle arrest ultimately leading to cellular senescence. Autophagy impairment is a hallmark of cellular aging, and the rescue of this proteostasis mechanism delays aging progression in HGPS cells. We have previously shown that the endogenous Neuropeptide Y (NPY) increases autophagy in hypothalamus, a brain area already identified as a central regulator of whole-body aging. We also showed that NPY mediates caloric restriction-induced autophagy. These results are in accordance with other studies suggesting that NPY may act as a caloric restriction mimetic and plays a role as a lifespan and aging regulator. The aim of the present study was, therefore, to investigate if NPY could delay HGPS premature aging phenotype. Herein, we report that NPY increases autophagic flux and progerin clearance in primary cultures of human dermal fibroblasts from HGPS patients. NPY also rescues nuclear morphology and decreases the number of dysmorphic nuclei, a hallmark of HGPS cells. In addition, NPY decreases other hallmarks of aging as DNA damage and cellular senescence. Altogether, these results show that NPY rescues several hallmarks of cellular aging in HGPS cells, suggesting that NPY can be considered a promising strategy to delay or block the premature aging of HGPS.
机译：Hutchinson-Gilford Progeria综合征（HGP或古典普鲁杰利症）是一种罕见的遗传障碍，其特征在于过早老化，并且由Lamin A / C基因（LMNA）内的De Novo Point突变（C608G）引起，产生异常的Lamin a蛋白质，称为progerin。 Progerin的积累会导致核异常和细胞周期逮捕最终导致细胞衰老。自噬障碍是细胞衰老的标志，并且该蛋白质抑制机制延迟了HGPS细胞中的老化进展。我们之前已经表明，内源性神经肽Y（NPY）增加了下丘脑中的自噬，已经被鉴定为全身衰老的中央调节器的脑区域。我们还表明，NPY介导卡路里限制诱导的自噬。这些结果符合其他研究，表明NPY可以充当热量限制模拟物并发挥作用作为寿命和老化调节器。因此，目前研究的目的是调查NPY是否可以延迟HGPS过早衰老表型。在此，我们认为NPY增加了HGPS患者的人皮肤成纤维细胞的原发性培养中的自噬助焊剂和普形酸葡萄球菌清除。 NPY还拯救了核形态并降低了疑风核的数量，HGPS细胞的标志。此外，NPY将其他衰老的其他标志降低，作为DNA损伤和细胞衰老。总而言之，这些结果表明，NPY拯救了HGPS细胞中细胞老化的几个标志，表明NPY可以被认为是延迟或阻止HGP过早老化的有希望的策略。

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