Effect of hypoxic preconditioning on brain genomic response before and following ischemia in the adult mouse: identification of potential neuroprotective candidates for stroke.

Yang Tang, Emilie Pacary, Thomas Fréret, Didier Divoux, Edwige Petit, Pascale Schumann-Bard, Myriam Bernaudin
Neurobiology of Disease. 2006-01-01; 21(1): 18-28
DOI: 10.1016/j.nbd.2005.06.002

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1. Neurobiol Dis. 2006 Jan;21(1):18-28. Epub 2005 Jul 22.

Effect of hypoxic preconditioning on brain genomic response before and following
ischemia in the adult mouse: identification of potential neuroprotective
candidates for stroke.

Tang Y(1), Pacary E, Fréret T, Divoux D, Petit E, Schumann-Bard P, Bernaudin M.

Author information:
(1)The M.I.N.D. Institute and Department of Neurology, University of California
at Davis, Davis, CA 95616, USA.

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% O2 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 (ATF3, C/EBPdelta). A second
wave of changes occurred 24 h 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, MTs, C/EBPdelta).

DOI: 10.1016/j.nbd.2005.06.002
PMID: 16040250 [Indexed for MEDLINE]

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