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Brain neovascularization determines functional recovery after intracerebral hemorrhage through the p53 signaling pathway

AuthorsRodríguez, Cristina CSIC ORCID; Carabias-Carrasco, Mónica; Resch-Beusher, Monica; Prieto, Estefanía; Almeida, Angeles CSIC ORCID CVN
Issue Date2019
Citation42ⁿᵈ Congress of the Spanish Society of Biochemistry and Molecular Biology (2019)
AbstractIntracerebral hemorrhage (ICH) is the most severe type of stroke and associates with high mortality rates and risk of disability of affected patients. So far there is no effective treatment, which, added to the lack of accurate prognosis, evidences the need to deepen the mechanisms that regulate brain repair after ICH.We previously shown that the human Tp53 Arg72Pro SNP modulates brain endothelial cells survival after ICH, which is essential for the secretion of growth factors and cytokines (i.e. VEGF) that mediate the mobilization of endothelial progenitor cells (EPCs) from the bone marrow to the peripheral blood. EPCs promote brain vascular repair after ICH, which is a vital response to restore oxygen supply and metabolic substrates in the ischemic brain. Then, pro-apoptotic p53 might be a negative regulator of EPC mobilization, thus affecting the functional prognosis after hemorrhagic stroke. Since p53 is accumulated in the brain after ICH, we speculate that p53 destabilization not only will promote cell survival, but also vascular recovery and brain repair. To con rm this hypothesis, p53 KO mice were subjected to an experimental in vivo model of ICH by injecting bacterial collagenase into the basal ganglia. We also analyzed proliferative markers and perfusion status of newlyformed brain blood vessels in the brain by Evans blue injection. We observed that p53 loss reduced lesion volume and increased levels of circulating EPCs. As a consequence, an improved vascular response was achieved in p53 KO mice, in comparison with those expressing an active p53 protein. Our results point out the impact of the p53 signaling pathway in the balance between brain damage and repair, which conditions functional recovery after ICH, suggesting p53 as a possible therapeutic target for hemorrhagic stroke.
DescriptionResumen del trabajo presentado al Spanish Society of Biochemistry and Molecular Biology (SEBBM), celebrado en Madrid del 16 al 19 de julio de 2019.
Appears in Collections:(IBFG) Comunicaciones congresos
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