Neuron-Specific Prolyl-4-Hydroxylase Domain 2 Knockout Reduces Brain Injury After Transient Cerebral Ischemia | Zendy

Reiner Kunze | Zendy; Wei Zhou | Zendy; Roland Veltkamp | Zendy; Ben Wielockx | Zendy; Georg Breier | Zendy; Hugo H. Marti | Zendy

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Neuron-Specific Prolyl-4-Hydroxylase Domain 2 Knockout Reduces Brain Injury After Transient Cerebral Ischemia

Author(s) -

Reiner Kunze,

Wei Zhou,

Roland Veltkamp,

Ben Wielockx,

Georg Breier,

Hugo H. Marti

Publication year - 2012

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/strokeaha.112.669598

Subject(s) - forebrain , erythropoietin , neuroprotection , medicine , ischemia , hypoxia (environmental) , hippocampal formation , endocrinology , microbiology and biotechnology , biology , central nervous system , chemistry , organic chemistry , oxygen

Numerous factors involved in the adaptive response to hypoxia, including erythropoietin and vascular endothelial growth factor are transcriptionally regulated by hypoxia-inducible factors (HIFs). During normoxia, prolyl-4-hydroxylase domain (PHD) proteins hydroxylate HIF-α subunits, resulting in their degradation. We investigated the effect of neuronal deletion of PHD2, the most abundant isoform in brain, for stroke outcome.

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