Journal
NEUROBIOLOGY OF DISEASE
Volume 21, Issue 1, Pages 18-28Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2005.06.002
Keywords
preconditioning; tolerance; hypoxia; ischemia; microarray; genomic; brain; therapeutical target; mouse; real-time PCR
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Funding
- NIA NIH HHS [AG19561] Funding Source: Medline
- NINDS NIH HHS [NS28167, NS42774] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS042774, R01NS028167] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R21AG019561] Funding Source: NIH RePORTER
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The aim of the present study is to better understand oxygen-sensitive adaptative pathways underlying the hypoxic preconditioning-induced protection of the brain against ischemia. Using oligonucleotide microarrays, we examined the brain genomic response of adult mice following hypoxia preconditioning (8% O-2 for 1 or 6 h of hypoxia with reoxygenation 12, 18, 24 h or 72 h) and ischemia (6 h), preceeded (tolerant state) or not, by preconditioning. Real-time PCR was used to validate the results. Most gene expression increases occurred during hypoxia, including those of HIF-1-dependent genes (RTP801, AM, VEGF, p21, GLUT-1), early response genes (IER3) and transcriptional factors (A TF3, C/EBP delta). A second wave of changes occurred 24 It after reoxygenation (S100A5, TH, Calretinin, PBX3). A third one occurred during ischemia itself, revealing that hypoxic preconditioning modifies the brain genomic response to ischemia. In addition, we show that some identical genes are overexpressed by hypoxia in both neonatal and adult brains (VEGF, EPO, GLUT-1, AM, MT5, CIEBP6). (c) 2005 Elsevier Inc. All rights reserved.
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