Aging of Hutchinson-Gilford progeria syndrome fibroblasts is characterised by hyperproliferation and increased apoptosis
Aging of Hutchinson-Gilford progeria syndrome fibroblasts is characterised by hyperproliferation and increased apoptosis
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DOI：
10.1016/j.exger.2004.02.002
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发表时间：
2004-05-01
影响因子：
3.9
通讯作者：
Kill, IR
中科院分区：
文献类型：
--
作者：
Bridger, JM;Kill, IR
哈钦森-吉尔福德早衰综合症是一种罕见的遗传性疾病，它模仿了过早衰老的某些方面。最近的研究表明，核纤层蛋白 A 基因的突变是导致这种疾病的一个原因。我们在此表明，哈钦森-吉尔福德早衰综合征成纤维细胞的细胞衰老的特征是一段时期的过度增殖，并以细胞凋亡率的大幅增加而终止。其他人报道的细胞核形态异常的细胞的出现被证明是细胞分裂的结果，因为这些异常的比例随着细胞年龄的增加而增加。同样，具有异常或缺失 A 型层的细胞比例随着年龄的增长而增加。这些数据为HGPS中过早衰老的细胞基础提供了线索，并支持了细胞衰老和组织稳态是正常衰老过程中重要因素的观点。 (C) 2004 Elsevier Inc. 保留所有权利。
Hutchinson-Gilford progeria syndrome is a rare genetic disorder that mimics certain aspects of aging prematurely. Recent work has revealed that mutations in the lamin A gene are a cause of the disease. We show here that cellular aging of Hutchinson-Gilford progeria syndrome fibroblasts is characterised by a period of hyperproliferation and terminates with a large increase in the rate of apoptosis. The occurrence of cells with abnormal nuclear morphology reported by others is shown to be a result of cell division since the fraction of these abnormalities increases with cellular age. Similarly, the proportion of cells with an abnormal or absent A-type lamina increases with age. These data provide clues as to the cellular basis for premature aging in HGPS and support the view that cellular senescence and tissue homeostasis are important factors in the normal aging process. (C) 2004 Elsevier Inc. All rights reserved.