UVB-induced premature senescence of human diploid skin fibroblasts

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Abstract

In this work, we show that repeated stresses with UVB (290-320nm) induce stress-induced premature senescence (SIPS) of skin human diploid fibroblasts (HDFs). HDFs at early cumulative population doublings were exposed three or five times to increasing subcytotoxic doses of UVB with one stress per day. After 2 days of recovery, several biomarkers of replicative senescence were established. First, there was an increase in the proportion of cells positive for senescence-associated β-galactosidase activity. Second, there was a loss of replicative potential as assessed by a very low level of [3H]-thymidine incorporation. Third, the steady-state level of the mRNA of three senescence-associated genes, i.e. fibronectin, osteonectin and SM22, was increased in HDFs at 72h after three and five exposures to UVB. In conclusion, these results suggest that it is possible to induce SIPS in HDFs after repeated exposures to subcytotoxic doses of UVB. This model could be used to test whether HDFs in UVB-induced premature senescence are able to promote epithelial cell growth and tumorigenesis in skin, as shown recently with HDFs in H2O2-induced premature senescence.

Original languageEnglish
Pages (from-to)1331-1339
Number of pages9
JournalThe international journal of Biochemistry & Cell biology
Volume34
Issue number11
DOIs
Publication statusPublished - 1 Nov 2002

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Fibroblasts
Diploidy
Skin
Cell Aging
Osteonectin
Galactosidases
Cell growth
Biomarkers
Fibronectins
Thymidine
Carcinogenesis
Genes
Epithelial Cells
Recovery
Messenger RNA
Growth
Population

Keywords

  • Fibroblasts
  • Stress-induced premature senescence
  • Tumorigenesis
  • UVB

Cite this

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title = "UVB-induced premature senescence of human diploid skin fibroblasts",
abstract = "In this work, we show that repeated stresses with UVB (290-320nm) induce stress-induced premature senescence (SIPS) of skin human diploid fibroblasts (HDFs). HDFs at early cumulative population doublings were exposed three or five times to increasing subcytotoxic doses of UVB with one stress per day. After 2 days of recovery, several biomarkers of replicative senescence were established. First, there was an increase in the proportion of cells positive for senescence-associated β-galactosidase activity. Second, there was a loss of replicative potential as assessed by a very low level of [3H]-thymidine incorporation. Third, the steady-state level of the mRNA of three senescence-associated genes, i.e. fibronectin, osteonectin and SM22, was increased in HDFs at 72h after three and five exposures to UVB. In conclusion, these results suggest that it is possible to induce SIPS in HDFs after repeated exposures to subcytotoxic doses of UVB. This model could be used to test whether HDFs in UVB-induced premature senescence are able to promote epithelial cell growth and tumorigenesis in skin, as shown recently with HDFs in H2O2-induced premature senescence.",
keywords = "Fibroblasts, Stress-induced premature senescence, Tumorigenesis, UVB",
author = "Florence Chainiaux and Magalhaes, {Joao Pedro} and Fran{\cc}ois Eliaers and Jos{\'e} Remacle and Olivier Toussaint",
year = "2002",
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AU - Chainiaux, Florence

AU - Magalhaes, Joao Pedro

AU - Eliaers, François

AU - Remacle, José

AU - Toussaint, Olivier

PY - 2002/11/1

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N2 - In this work, we show that repeated stresses with UVB (290-320nm) induce stress-induced premature senescence (SIPS) of skin human diploid fibroblasts (HDFs). HDFs at early cumulative population doublings were exposed three or five times to increasing subcytotoxic doses of UVB with one stress per day. After 2 days of recovery, several biomarkers of replicative senescence were established. First, there was an increase in the proportion of cells positive for senescence-associated β-galactosidase activity. Second, there was a loss of replicative potential as assessed by a very low level of [3H]-thymidine incorporation. Third, the steady-state level of the mRNA of three senescence-associated genes, i.e. fibronectin, osteonectin and SM22, was increased in HDFs at 72h after three and five exposures to UVB. In conclusion, these results suggest that it is possible to induce SIPS in HDFs after repeated exposures to subcytotoxic doses of UVB. This model could be used to test whether HDFs in UVB-induced premature senescence are able to promote epithelial cell growth and tumorigenesis in skin, as shown recently with HDFs in H2O2-induced premature senescence.

AB - In this work, we show that repeated stresses with UVB (290-320nm) induce stress-induced premature senescence (SIPS) of skin human diploid fibroblasts (HDFs). HDFs at early cumulative population doublings were exposed three or five times to increasing subcytotoxic doses of UVB with one stress per day. After 2 days of recovery, several biomarkers of replicative senescence were established. First, there was an increase in the proportion of cells positive for senescence-associated β-galactosidase activity. Second, there was a loss of replicative potential as assessed by a very low level of [3H]-thymidine incorporation. Third, the steady-state level of the mRNA of three senescence-associated genes, i.e. fibronectin, osteonectin and SM22, was increased in HDFs at 72h after three and five exposures to UVB. In conclusion, these results suggest that it is possible to induce SIPS in HDFs after repeated exposures to subcytotoxic doses of UVB. This model could be used to test whether HDFs in UVB-induced premature senescence are able to promote epithelial cell growth and tumorigenesis in skin, as shown recently with HDFs in H2O2-induced premature senescence.

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