Reference : Role of Prion protein in premature senescence of human fibroblasts
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
http://hdl.handle.net/2268/253286
Role of Prion protein in premature senescence of human fibroblasts
English
Boilan, E. [Unité de Recherche en Biologie Cellulaire (URBC) - Namur Research Institute for Life Sciences (Narilis), University of Namur, Belgium, CESI, Chaussée de Louvain 290, 5004 Bouge, Belgium]
Winant, V. [Unité de Recherche en Biologie Cellulaire (URBC) - Namur Research Institute for Life Sciences (Narilis), University of Namur, Belgium]
Dumortier, E. [Unité de Recherche en Biologie Cellulaire (URBC) - Namur Research Institute for Life Sciences (Narilis), University of Namur, Belgium]
Elmoualij, Benaïssa mailto [Université de Liège - ULiège > Département des sciences biomédicales et précliniques > Histologie >]
Quatresooz, Pascale mailto [Université de Liège - ULiège > Département des sciences biomédicales et précliniques > Histologie >]
Osiewacz, H. D. [Institute of Molecular Biosciences, Johann Wolfgang Goethe University, Frankfurt am Main, Germany]
Debacq-Chainiaux, F. [Unité de Recherche en Biologie Cellulaire (URBC) - Namur Research Institute for Life Sciences (Narilis), University of Namur, Belgium]
Toussaint, O. [Unité de Recherche en Biologie Cellulaire (URBC) - Namur Research Institute for Life Sciences (Narilis), University of Namur, Belgium]
2017
Mechanisms of Ageing and Development
Elsevier Ireland Ltd
Yes (verified by ORBi)
0047-6374
[en] Copper ; Fibroblasts ; Oxidative stress ; Prion protein ; Senescence
[en] 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 (PrPC) into an infectious and disease-associated misfolded form, called scrapie isoform (PrPSc). Although its sequence is highly conserved, less information is available on its physiological role under normal conditions. However, increasing evidence supports a role for PrPC in the cellular response to oxidative stress. In the present study, a new link between PrP and senescence is highlighted. The role of PrP in premature senescence induced by copper was investigated. WI-38 human fibroblasts were incubated with copper sulfate (CuSO4) to trigger premature senescence. This induced an increase of PrP mRNA level, an increase of protein abundance of the normal form of PrP and a nuclear localization of the protein. Knockdown of PrP expression using specific small interfering RNA (siRNA) gave rise to appearance of several biomarkers of senescence as a senescent morphology, an increase of senescence associated β-galactosidase activity and a decrease of the cellular proliferative potential. Overall these data suggest that PrP protects cells against premature senescence induced by copper. © 2017 Elsevier B.V.
http://hdl.handle.net/2268/253286
10.1016/j.mad.2017.08.002

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