The Neuronal Ischemic Tolerance Is Conditioned by the Tp53 Arg72Pro Polymorphism View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-04

AUTHORS

Maria E. Ramos-Araque, Cristina Rodriguez, Rebeca Vecino, Elisa Cortijo Garcia, Mercedes de Lera Alfonso, Mercedes Sanchez Barba, Laura Colàs-Campàs, Francisco Purroy, Juan F. Arenillas, Angeles Almeida, Maria Delgado-Esteban

ABSTRACT

Cerebral preconditioning (PC) confers endogenous brain protection after stroke. Ischemic stroke patients with a prior transient ischemic attack (TIA) may potentially be in a preconditioned state. Although PC has been associated with the activation of pro-survival signals, the mechanism by which preconditioning confers neuroprotection is not yet fully clarified. Recently, we have described that PC-mediated neuroprotection against ischemic insult is promoted by p53 destabilization, which is mediated by its main regulator MDM2. Moreover, we have previously described that the human Tp53 Arg72Pro single nucleotide polymorphism (SNP) controls susceptibility to ischemia-induced neuronal apoptosis and governs the functional outcome of patients after stroke. Here, we studied the contribution of the human Tp53 Arg72Pro SNP on PC-induced neuroprotection after ischemia. Our results showed that cortical neurons expressing the Pro72-p53 variant exhibited higher PC-mediated neuroprotection as compared with Arg72-p53 neurons. PC prevented ischemia-induced nuclear and cytosolic p53 stabilization in Pro72-p53 neurons. However, PC failed to prevent mitochondrial p53 stabilization, which occurs in Arg72-p53 neurons after ischemia. Furthermore, PC promoted neuroprotection against ischemia by controlling the p53/active caspase-3 pathway in Pro72-p53, but not in Arg72-p53 neurons. Finally, we found that good prognosis associated to TIA within 1 month prior to ischemic stroke was restricted to patients harboring the Pro72 allele. Our findings demonstrate that the Tp53 Arg72Pro SNP controls PC-promoted neuroprotection against a subsequent ischemic insult by modulating mitochondrial p53 stabilization and then modulates TIA-induced ischemic tolerance. More... »

PAGES

204-215

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s12975-018-0631-1

DOI

http://dx.doi.org/10.1007/s12975-018-0631-1

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1103607736

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29687302


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