Cardiff University | Prifysgol Caerdydd ORCA
Online Research @ Cardiff 
WelshClear Cookie - decide language by browser settings

Prevention of accelerated cell aging in Werner syndrome using a p38 mitogen-activated protein kinase inhibitor

Davis, Terence, Baird, Duncan Martin, Haughton, Michele Fleur, Jones, Christopher John and Kipling, David Glyn 2005. Prevention of accelerated cell aging in Werner syndrome using a p38 mitogen-activated protein kinase inhibitor. The Journals of Gerontology. Series A: Biological Sciences and Medical Sciences 60 (11) , pp. 1386-93.

Full text not available from this repository.

Abstract

We investigated the role of p38 mitogen-activated protein kinase (MAPK) signalling in the accelerated aging of Werner Syndrome (WS) fibroblasts by use of SB203580, a cytokine-suppressive anti-inflammatory drug that targets p38 activity. SB203580 treatment reverts the aged morphology of young WS fibroblasts to that seen in young normal fibroblasts. In addition, SB203580 increases the life span and growth rate of WS fibroblasts to within the normal range. In young WS cells, p38 is activated coincident with an up-regulation of p21WAF1, and a reduction in the levels of both activated p38 and p21WAF1 are seen following treatment with SB203580. As these effects are not seen in young normal cells, our data suggest that the abbreviated replicative life span of WS cells is due to a stress-induced, p38-mediated growth arrest that is independent of telomere erosion. With some p38 inhibitors already in clinical trials, our data suggest a potential route to drug intervention in a premature aging syndrome.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
ISSN: 1079-5006
Last Modified: 18 Oct 2017 08:16
URI: http://orca.cf.ac.uk/id/eprint/191

Citation Data

Cited 66 times in Google Scholar. View in Google Scholar

Cited 74 times in Scopus. View in Scopus. Powered By Scopus® Data

Actions (repository staff only)

Edit Item Edit Item