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RESEARCH PRODUCT
Neuroglobin mRNA expression after transient global brain ischemia and prolonged hypoxia in cell culture.
Thorsten BurmesterMark HaberkampRainald Schmidt-kastnerThomas HankelnChristoph Schmitzsubject
MaleVascular Endothelial Growth Factor APathologymedicine.medical_specialtyCell SurvivalIschemiaNeuroglobinNerve Tissue ProteinsIn situ hybridizationBiologyPC12 CellsBrain ischemiaOxygen ConsumptionGene expressionmedicineAnimalsHumansRNA MessengerRats WistarMolecular BiologyCells CulturedIn Situ HybridizationNeuronsReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceHypoxia (medical)medicine.diseaseCell HypoxiaCell biologyGlobinsRatsRespiratory proteinCell cultureIschemic Attack TransientNeuroglobinNeurology (clinical)medicine.symptomDevelopmental Biologydescription
Abstract Neuroglobin is a nerve-specific respiratory protein that has been proposed to play an important role in the protection of brain neurons from ischemic and hypoxic injuries. Here, we investigated the regulation of neuroglobin expression after transient global ischemia in the rat brain using mRNA in situ hybridization and under hypoxic stress in cultured neuronal cell lines (PC12, HN33) by quantitative RT-PCR. While neuroglobin mRNA expression was significantly enhanced in cell culture after severe prolonged hypoxia (0–1% O 2 for 24 h), we did not find any significant increases in neuroglobin mRNA levels in the rat brain after transient global ischemia. Vegf and Glut1 mRNAs showed increases in the hippocampus as expected. Therefore, it is unlikely that neuroglobin is instrumental in the acute response of neurons to hypoxic or ischemic insults, for which the mammalian brain is not adapted.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2006-08-01 | Brain research |