Abstract
To test the involvement of the telomeres in the senescent phenotype, we used telomerase-immortalized human foreskin fibroblasts (hTERT-BJ1). We exposed hTERT-BJ1 and parental BJ cells to either UVB or H(2)O(2) subcytotoxic stress(es). Both cell lines developed biomarkers of replicative senescence: loss of replicative potential, increase in senescence-associated beta-galactosidase activity, typical senescence-like morphology, overexpression of p21(WAF-1) and p16(INK-4a), and decreased level of the hyperphosphorylated form of pRb. Telomere shortening was slightly higher under stress for both BJ and hTERT-BJ1 but still much lower than that reported for other cell lines. We conclude that pathways alternative to telomere shortening must cause the appearance of the senescence phenotype.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cell Line
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Cellular Senescence / physiology*
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Cyclin-Dependent Kinase Inhibitor p16 / analysis
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Cyclin-Dependent Kinase Inhibitor p16 / metabolism
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Cyclin-Dependent Kinase Inhibitor p21
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Cyclins / analysis
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Cyclins / metabolism
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Fibroblasts / drug effects
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Fibroblasts / physiology*
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Fibroblasts / radiation effects
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Humans
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Hydrogen Peroxide / pharmacology*
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Phosphorylation
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Retinoblastoma Protein / analysis
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Retinoblastoma Protein / metabolism
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Skin / pathology
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Stress, Physiological / pathology*
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Telomerase / genetics
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Telomerase / metabolism
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Telomere / drug effects
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Telomere / physiology*
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Telomere / radiation effects
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Transfection
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Tumor Suppressor Protein p53 / analysis
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Tumor Suppressor Protein p53 / metabolism
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Ultraviolet Rays / adverse effects*
Substances
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CDKN1A protein, human
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Cyclin-Dependent Kinase Inhibitor p16
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Cyclin-Dependent Kinase Inhibitor p21
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Cyclins
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Retinoblastoma Protein
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Tumor Suppressor Protein p53
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Hydrogen Peroxide
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Telomerase