Suppression subtraction hybridization and northern analysis reveal upregulation of heat shock, trkB, and sodium calcium exchanger genes following global cerebral ischemia in the rat

Driver (sham-operated) and tester (ischemic) hippocampal cDNAs were subtracted, and the resulting ischemia-induced upregulated gene expression was verified by northern analysis. cDNAs isolated corresponded to (1) genes known to be upregulated following ischemia, (hsc70, hsp90, hsp105 and trkB) and (...

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Veröffentlicht in:	Brain research. Molecular brain research. 2001-09, Vol.93 (2), p.173-179
Hauptverfasser:	Majda, Bernadette T, Meloni, Bruno P, Rixon, Nerida, Knuckey, Neville W
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Biological and medical sciences Blotting, Northern Brain Ischemia - genetics Brain Ischemia - metabolism DNA, Complementary - genetics Gene Expression Profiling - methods Gene Expression Regulation Heat shock protein Heat-Shock Proteins - biosynthesis Heat-Shock Proteins - genetics Hippocampus - metabolism Ischemic Attack, Transient - genetics Ischemic Attack, Transient - metabolism Ischemic tolerance Male Medical sciences ncx gene Nerve Tissue Proteins - biosynthesis Nerve Tissue Proteins - genetics Neurology Rats Rats, Sprague-Dawley Receptor, trkB - biosynthesis Receptor, trkB - genetics Sodium calcium exchanger Sodium-Calcium Exchanger - biosynthesis Sodium-Calcium Exchanger - genetics Subtraction Technique Suppression subtraction hybridization Up-Regulation Vascular diseases and vascular malformations of the nervous system
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Zusammenfassung:	Driver (sham-operated) and tester (ischemic) hippocampal cDNAs were subtracted, and the resulting ischemia-induced upregulated gene expression was verified by northern analysis. cDNAs isolated corresponded to (1) genes known to be upregulated following ischemia, (hsc70, hsp90, hsp105 and trkB) and (2) a gene not previously implicated with cerebral ischemia, sodium calcium exchanger (ncx). Furthermore, upregulation of these genes was demonstrated following preconditioning transient global ischemia.
ISSN:	0169-328X 1872-6941
DOI:	10.1016/S0169-328X(01)00203-0