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Erythropoietin: A Neuroprotective Agent in Cerebral Hypoxia, Neurodegeneration, and Epilepsy

[ Vol. 19 , Issue. 38 ]

Author(s):

Amalia Merelli, Liliana Czornyj and Alberto Lazarowski   Pages 6791 - 6801 ( 11 )

Abstract:


Neuronal damage secondary to brain injuries such as cerebral hypoxia, seizures as well as neurodegenerative process, may include pro-inflammatory changes. The activation of a common mechanism related to survival or cell death, mediated by the stabilization and trans-activation of Hypoxia-Inducible Factor 1 (HIF-1), has been observed in these conditions. HIF-1 may induce over expression of P-glycoprotein, the product multidrug-resistance gene (MDR-1), both on blood-brain barrier as well as on the cerebral damaged cells, producing the refractoriness to therapeutic strategies for neuroprotection. However, in these same cells, HIF-1 can also induce the expression of erythropoietin receptor (Epo-R). Irrespective of its known properties on hematopoiesis, it was proposed that erythropoietin can trigger neuroprotective mechanisms mediated by Epo-R activation. Brain hypoxia, epilepsy, neurodegeneration and inflammation, can share the induction of Epo-R and several other growth factor receptors as well as signal transductions pathways after HIF-1 transactivation. Perhaps, the use of the intranasal route for the exogenous administration of Epo, (or other biological compounds) could help neuroprotection as well as to repair the brain areas damaged.

Keywords:

Cerebral hypoxia, neurodegenration, refractory epilepsy, erythropoietin, HIF-1, P-Glycoprotein

Affiliation:

Instituto de Investigaciones en Fisiopatología y Bioquímica Clínica (INFIBIOC), Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires (UBA), Junín 956, C1121ABGBuenos Aires, Argentina



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