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• W2022996558 abstract "Hypoxic–ischemic brain injury is regulated in part by neurotransmitter and chemokine signaling via G-protein-coupled receptors (GPCRs). GPCR-kinase 2 (GRK2) protects these receptors against overstimulation by inducing desensitization. Neonatal hypoxic–ischemic brain damage is preceded by a reduction in cerebral GRK2 expression. We determined the functional importance of GRK2 in hypoxic–ischemic brain damage. Nine-day-old wild-type and GRK2 +/− mice with a ∼50% reduction in GRK2 protein were exposed to unilateral carotid artery occlusion and hypoxia. In GRK2 +/− animals, gray and white matter damage was aggravated at 3 weeks after hypoxia–ischemia. In addition, cerebral neutrophil infiltration was increased in GRK2 +/− animals. Neutrophil depletion reduced brain damage, but neuronal loss was still more pronounced in GRK2 +/− animals. Onset of neuronal loss was advanced in GRK2 +/− animals regardless of neutrophil depletion. White matter injury was advanced in GRK2 +/− animals and was not affected by neutrophil depletion. Activation/infiltration of microglia/macrophages was stronger in GRK2 +/− brains but only occurred 24 h after hypoxia–ischemia and is therefore not the primary cause of increased damage. During hypoxia, cerebral blood flow was reduced to the same extent in both genotypes. In vitro , GRK2 +/− hippocampal slices and cerebellar granular neurons were more sensitive to glutamate-induced death. We propose the novel concept that the kinase GRK2 regulates onset and magnitude of hypoxic–ischemic brain damage. Increased gray and white matter damage in GRK2 +/− animals was not dependent on infiltrating neutrophils and occurred before microglia/macrophage activation was detected. Collectively, our data suggest that cerebral GRK2 has an important endogenous neuroprotective role in ischemic cerebral damage." @default.
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• W2022996558 date "2008-03-26" @default.
• W2022996558 modified "2023-10-11" @default.
• W2022996558 title "Low Endogenous G-Protein-Coupled Receptor Kinase 2 Sensitizes the Immature Brain to Hypoxia–Ischemia-Induced Gray and White Matter Damage" @default.
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• W2022996558 doi "https://doi.org/10.1523/jneurosci.4769-07.2008" @default.
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