ArticleCellular and molecular life sciences : CMLS2011
Enhanced susceptibility of T lymphocytes to oxidative stress in the absence of the cellular prion protein.
Article in Cellular and molecular life sciences : CMLS, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Stress Resilience of Spermatozoa and Blood Mononuclear Cells without Prion Protein.Frontiers in molecular biosciences · 2018Article
- Gene expression resulting from PrPC ablation and PrPC overexpression in murine and cellular models.Molecular neurobiology · 2014Review
- Deoxycytidine kinase augments ATM-Mediated DNA repair and contributes to radiation resistance.PloS one · 2014Article
- Molecular responses of mouse macrophages to copper and copper oxide nanoparticles inferred from proteomic analyses.Molecular & cellular proteomics : MCP · 2013Article
- Ablation of the cellular prion protein, PrPC, specifically on follicular dendritic cells has no effect on their maturation or function.Immunology · 2013Article
- Recruitment of cellular prion protein to mitochondrial raft-like microdomains contributes to apoptosis execution.Molecular biology of the cell · 2011Article
- Neuroprotective role of PrPC against kainate-induced epileptic seizures and cell death depends on the modulation of JNK3 activation by GluR6/7-PSD-95 binding.Molecular biology of the cell · 2011Article
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8 authors.
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Abstract
The cellular prion glycoprotein (PrP(C)) is ubiquitously expressed but its physiologic functions remain enigmatic, particularly in the immune system. Here, we demonstrate in vitro and in vivo that PrP(C) is involved in T lymphocytes response to oxidative stress. By monitoring the intracellular level of reduced glutathione, we show that PrP(-/-) thymocytes display a higher susceptibility to H(2)O(2) exposure than PrP(+/+) cells. Furthermore, we find that in mice fed with a restricted diet, a regimen known to increase the intracellular level of ROS, PrP(-/-) thymocytes are more sensitive to oxidative stress. PrP(C) function appears to be specific for oxidative stress, since no significant differences are observed between PrP(-/-) and PrP(+/+) mice exposed to other kinds of stress. We also show a marked evolution of the redox status of T cells throughout differentiation in the thymus. Taken together, our results clearly ascribe to PrP(C) a protective function in thymocytes against oxidative stress.
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