期刊
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
卷 66, 期 4, 页码 367-375出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/gerona/glq197
关键词
Aging; Replicative senescence; H2AX; DNA double-strand break repair; Fibroblasts; Growth inhibition
资金
- Australian National Health
- Medical Research Council [606614, 145780, 288713]
- Australian National Breast Cancer Foundation
- Victorian Government
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 gamma H2AX 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 gamma H2AX 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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据