Induction of c-Fos, junB, c-Jun, and hsp70 mRNA in Cortex, Thalamus, Basal Ganglia, and Hippocampus following Middle Cerebral Artery Occlusion

Abstract

Middle cerebral artery (MCA) occlusion in halothane-anesthetized rats induced c-fos, junB, and c-jun immediate early gene mRNAs and hsp70 heat shock gene mRNA in brain. In situ hybridization studies showed that c-fos and junB were induced throughout all of the cortex at 1 and 4 h following MCA occlusion. hsp70 was induced in the core and margins of the MCA ischemia. By 24 h, there was little expression of c-fos, junB, c-jun, and hsp70 in the core of the MCA infarct; there was modest induction of hsp70 at the margins of the infarct; and there was diffuse induction of c-fos, junB, and c-jun in all of the cortex outside the infarct. MCA occlusion also induced these genes in subcortical structures. c-fos, junB, and hsp70 were induced in ipsilateral medial striatum, most of thalamus including medial and lateral geniculate nuclei, substantia nigra, and hippocampus. Most of these structures, except for the striatum, are not supplied by the MCA. These data show that changes in gene expression can occur in regions remote from an infarction.

Genome-Wide Gene Expression Analysis for Induced Ischemic Tolerance and Delayed Neuronal Death following Transient Global Ischemia in Rats

“…dictory observations have been reported that mRNA for c-Fos and JunB were widely expressed in the surviving peri-infarct area after focal ischemia (Kinouchi et al, 1994). Consistent with our observations, c-Fos and c-Jun have been shown to be up-regulated in sublethal ischemia (Sommer et al, 1995;Truettner et al, 2002) and spreading depression (Kariko et al, 1998), that renders brain resistant to ischemic injury (Kawahara et al, 1995;Kirino et al, 1991).…”

Cluster analysis of mrna expression levels identifies multiple sequential patterns following focal cerebral ischemia

“…This study shows that c-fos mRNA significantly increases during the hyperacute phase after focal cerebral ischemia. Needless to say, c-fos is an immediate early gene (IEG) that is activated immediately after certain kinds of cellular insults, as well as following focal cerebral ischemia (1,6). IEGs play key roles in starting many genetic cascades.…”

Thinning, movement, and volume loss of residual cortical tissue occurs after stroke in the adult rat as identified by histological and magnetic resonance imaging analysis

“…During ischemia, general protein synthesis (Thilmann et al, 1986), and gene expression (Nowak, 1985;Jacewitz et al, 1986) are suppressed in the penumbra, such that only select groups of proteins such as heat shock proteins (Lindquist and Craig, 1988), immediate early genes (Kinouchi et al, 1994), neurotropins (Lindvall et al, 1992), and some apoptosis genes (Chen et al, 1995) are expressed. Some of these gene products may lead to cell death, but others can help injured neurons survive the recovery process.…”