TY - JOUR
T1 - Detailed analysis of DNA repair and senescence marker kinetics over the life span of a human fibroblast cell line
AU - Endt, Heidrun
AU - Sprung, Carl
AU - Keller, Ulrike
AU - Gaipl, Udo
AU - Fietkau, Rainer
AU - Distel, Luitpold
PY - 2011
Y1 - 2011
N2 - We examined phosphorylation of H2AX, a marker for DNA double-strand breaks over the life of a human fibroblast cell line. This marker was compared with a number of other cellular senescence and DNA repair endpoints. An increase in gammaH2AX foci number was observed after 24 hours of repair time following DNA damage over the course of fibroblast passaging. Progressive and relatively constant changes in growth retardation, doubling time, and telomere length were also observed. The fraction of cells expressing beta-gal, a marker of cellular senescence, increased considerably around the 40th passage as did some other cell morphology endpoints. The detectable gammaH2AX foci at 24 hours after ionizing radiation were far fewer than the number detected at 1 hour across all passage numbers. We conclude that although residual DNA damage level increases with passage number, it is unlikely to be the result of less efficient DNA repair in the aged fibroblast since most DNA damage is repaired, even at late passages.
AB - We examined phosphorylation of H2AX, a marker for DNA double-strand breaks over the life of a human fibroblast cell line. This marker was compared with a number of other cellular senescence and DNA repair endpoints. An increase in gammaH2AX foci number was observed after 24 hours of repair time following DNA damage over the course of fibroblast passaging. Progressive and relatively constant changes in growth retardation, doubling time, and telomere length were also observed. The fraction of cells expressing beta-gal, a marker of cellular senescence, increased considerably around the 40th passage as did some other cell morphology endpoints. The detectable gammaH2AX foci at 24 hours after ionizing radiation were far fewer than the number detected at 1 hour across all passage numbers. We conclude that although residual DNA damage level increases with passage number, it is unlikely to be the result of less efficient DNA repair in the aged fibroblast since most DNA damage is repaired, even at late passages.
UR - http://biomedgerontology.oxfordjournals.org/content/66A/4/367.full.pdf+html
U2 - 10.1093/gerona/glq197
DO - 10.1093/gerona/glq197
M3 - Article
SN - 1079-5006
VL - 66
SP - 367
EP - 375
JO - The Journals of Gerontology, Series A: Biological Sciences and Medical Sciences
JF - The Journals of Gerontology, Series A: Biological Sciences and Medical Sciences
IS - 4
ER -