Prevention of accelerated cell aging in the Werner syndrome

Davis, Terence ORCID: https://orcid.org/0000-0003-2780-0262, Haughton, Michele F., Jones, Christopher J. and Kipling, David Glyn 2006. Prevention of accelerated cell aging in the Werner syndrome. Annals of the New York Academy of Sciences 1067 (1) , pp. 243-247. 10.1196/annals.1354.031

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Abstract

n 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 p21WAF1 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.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Medicine
Subjects:	R Medicine > R Medicine (General)
Uncontrolled Keywords:	actin stress fibers; p21WAF1; p38 MAPK; p53; SB203580; senescence; telomeres; telomerase; Werner syndrome
Publisher:	Wiley-Blackwell
ISSN:	0077-8923
Last Modified:	14 Dec 2022 02:15
URI:	https://orca.cardiff.ac.uk/id/eprint/46699

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