| Autor: |
Kleszka K; Institute of Physiology, University Duisburg-Essen, Essen, Germany., Leu T; Institute of Physiology, University Duisburg-Essen, Essen, Germany., Quinting T; Institute of Physiology, University Duisburg-Essen, Essen, Germany., Jastrow H; Institute of Anatomy and Institute for Experimental Immunology and Imaging, Imaging Centre Essen, Electron Microscopy Unit, Essen University Hospital, Essen, Germany., Pechlivanis S; Institute for Medical Informatics, Biometry and Epidemiology, University Hospital of Essen, University Duisburg-Essen, Essen, Germany., Fandrey J; Institute of Physiology, University Duisburg-Essen, Essen, Germany. joachim.fandrey@uni-due.de., Schreiber T; Institute of Physiology, University Duisburg-Essen, Essen, Germany.; Department of Physiology, Pathophysiology and Toxicology and Center for Biomedical Education and Research (ZBAF), University of Witten/Herdecke, 58453, Witten, Germany. |
| Abstrakt: |
Sufficient tissue oxygenation is required for regular brain function; thus oxygen supply must be tightly regulated to avoid hypoxia and irreversible cell damage. If hypoxia occurs the transcription factor complex hypoxia-inducible factor (HIF) will accumulate and coordinate adaptation of cells to hypoxia. However, even under atmospheric O 2 conditions stabilized HIF-2α protein was found in brains of adult mice. Mice with a neuro-specific knockout of Hif-2α showed a reduction of pyramidal neurons in the retrosplenial cortex (RSC), a brain region responsible for a range of cognitive functions, including memory and navigation. Accordingly, behavioral studies showed disturbed cognitive abilities in these mice. In search of the underlying mechanisms for the specific loss of pyramidal cells in the RSC, we found deficits in migration in neural stem cells from Hif-2α knockout mice due to altered expression patterns of genes highly associated with neuronal migration and positioning. |
