Saretzki G, Feng J, von Zglinicki T, Villeponteau B
Institute of Pathology, Charité, Humboldt-University Berlin, Germany.
J Gerontol A Biol Sci Med Sci. 1998 Nov;53(6):B438-42. doi: 10.1093/gerona/53a.6.b438.
Different DNA-damaging treatments produce a senescence-like phenotype. Young human fibroblasts are transferred to a senescence-like state after 4 to 6 weeks of culture under 40% ambient oxygen partial pressure. In order to understand the causes of senescence it would be advantageous to know how well this state equals accelerated senescence. Therefore, we measured the expression of genes with known senescence-specific expression pattern in human fibroblasts, which were irreversibly proliferation-inhibited by chronic hyperoxic treatment. A senescence-specific gene expression pattern was confirmed by semiquantitative RT-PCR for eight out of nine examined genes in BJ foreskin fibroblasts and for four out of four genes in MRC-5 lung fibroblasts. For all these cases, gene expression under hyperoxia was similar to that in senescent cells, suggesting that chronic mild hyperoxia is a valid model for accelerated senescence.
