Role of Prion protein in premature senescence of human fibroblasts.

Prion protein (PrP) is essentially known for its capacity to induce neurodegenerative prion diseases in mammals caused by a conformational change in its normal cellular isoform (PrP) into an infectious and disease-associated misfolded form, called scrapie isoform (PrP). Although its sequence is highly conserved, less information is available on its physiological role under normal conditions. However, increasing evidence supports a role for PrP in the cellular response to oxidative stress.

Role of p38MAPK and oxidative stress in copper-induced senescence.

In the present work, we indicate that copper is involved in the senescence of human diploid fibroblasts and we describe mechanisms to explain it. Using different techniques, we show for the first time an accumulation of copper in cells during replicative senescence. This accumulation seems to be co-localized with lipofuscin.