Prevention of Accelerated Cell Aging in the Werner Syndrome

被引：30

作者：

Davis, Terence ^{[1
]}

Haughton, Michele F. ^{[1
]}

Jones, Christopher J. ^{[1
]}

Kipling, David ^{[1
]}

机构：

[1] Cardiff Univ, Dept Pathol, Sch Med, Cardiff CF14 4XN, S Glam, Wales

来源：

UNDERSTANDING AND MODULATING AGING | 2006年 / 1067卷

基金：

英国生物技术与生命科学研究理事会;

关键词：

actin stress fibers; p21(WAF1); p38; MAPK; p53; SB203580; senescence; telomeres; telomerase; Werner syndrome;

D O I：

10.1196/annals.1354.031

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

In the Werner syndrome (WS) fibroblasts have an increased life span and growth rate when treated with the p38 inhibitor SB203580. Additionally, the cellular morphology reverts to that seen in young normal fibroblasts. The p38 pathway is activated in young WS cells, associated with high levels of p21(WAF1) leading to cell cycle arrest, and is suppressed by SB203580. As these changes are also seen in telomerized WS cells, these data show that the growth problems seen in WS cells, and perhaps the accelerated in vivo aging, are due to a telomere-independent premature senescence mechanism. The suppression of this mechanism by SB203580 treatment suggests a route whereby WS may be amenable to therapeutic intervention.

引用

页码：243 / 247

页数：5

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