X-Message-Number: 27807
Date: Tue, 4 Apr 2006 20:25:27 -0700 (PDT)
From: Doug Skrecky <>
Subject: premature aging of Werner syndrome blocked

[There is a possibility that the lifespan of those suffering from Werner
premature aging syndrome may soon be increased to the "normal" range.]

J Gerontol A Biol Sci Med Sci. 2005 Nov;60(11):1386-93.
Prevention of accelerated cell aging in Werner syndrome using a p38
mitogen-activated protein kinase inhibitor.
  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 p21(WAF1),
and a reduction in the levels of both activated p38 and p21(WAF1) 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.

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