scholarly journals Global Ischemia Induces Immediate-Early Genes Encoding Zinc Finger Transcription Factors

1996 ◽  
Vol 16 (4) ◽  
pp. 557-565 ◽  
Author(s):  
Jari Honkaniemi ◽  
Frank R. Sharp
Keyword(s):  
Transcription Factors ◽  
Dentate Gyrus ◽  
Neuronal Death ◽  
Immediate Early Genes ◽  
Global Ischemia ◽  
Immediate Early ◽  
Mrna Levels ◽  
Brain Areas ◽  
Ca1 Neurons ◽  
Early Genes

Ischemia induces immediate-early genes (IEGs) in brain. Since prolonged expression of some IEGs may precede neuronal death, some researchers have suggested that these IEGs mediate neuronal death. We therefore examined the effect of 5 and 10 min of global ischemia on the expression of the IEGs NGFI-A, NGFI-B, NGFI-C, egr-2, egr-3, and Nurr1 in gerbil brain. All of the IEGs were induced after 30 min of reperfusion in the hippocampus. Most of them were induced in several other regions as well, including cortex, hypothalamus, thalamus, and amygdala. The acute IEG induction decreased in most brain areas by 2–6 h. However, at 24 h following 5 min of ischemia NGFI-A continued to be expressed in the CA1 region and dentate gyrus. In the dentate gyrus, NGFI-C continued to be expressed for 24 h and egr-3 for as long as 72 h. In other brain areas, all of the IEGs returned to control levels by 72 h except in CA1, where most messenger RNA (mRNA) levels were decreased; this decrease correlated with marked neuronal loss. The persistent expression of NGFI-A in CA1 neurons destined to die and the persistent expression of NGFI-A, NGFI-C, and egr-3 genes in dentate granule cell neurons that survive may indicate that some transcription factors modulate cell death whereas others support cell survival when expressed for prolonged periods. The protein products of several transcription factors, including c- fos, are known to downregulate their own expression. The persistent expression of NGFI-A in the CA1 neurons destined to die could therefore be due to ischemia-induced transcriptional activation caused by, e.g., increased intracellular calcium levels plus a lack of negative feedback caused by the blockade of the translation of NGFI-A mRNA into protein.

scholarly journals Differential Expression of the Immediate Early Genes c-Fos, c-Jun, JunB, and NGFI-B in the Rat Brain following Transient Forebrain Ischemia

1994 ◽  
Vol 14 (2) ◽  
pp. 206-216 ◽  
Author(s):  
Tobias Neumann-Haefelin ◽  
Christoph Wießner ◽  
Peter Vogel ◽  
Tobias Back ◽  
Konstantin-Alexander Hossmann
Keyword(s):  
Metabolic Response ◽  
Late Onset ◽  
Immediate Early Genes ◽  
Selective Vulnerability ◽  
Brain Regions ◽  
Global Ischemia ◽  
Immediate Early ◽  
Mrna Levels ◽  
Early Genes ◽  
Ca1 Region

The temporospatial expression pattern of four immediate early genes (IEGs) (c- fos, c- jun, junB, NGFI-B) following 30 min of global ischemia was investigated in rat brains by in situ hybridization and immunohistochemistry (c- fos). All examined IEG mRNAs, as well as Fos-like immunoreactivity, increased transiently in vulnerable and resistant brain regions following ischemia, but the induction profiles were distinct. Ischemia caused a post-ischemic early-onset, transient c- fos induction in widespread regions, as well as a late-onset induction restricted to vulnerable regions. Late-onset c- fos induction was observed in the CA1 region and the ventral thalamus but not in the striatum or neocortex, where neurons degenerate at a quicker pace. After recirculation, c- jun mRNA appeared to be initially coinduced with c- fos mRNA, but c- jun mRNA levels remained elevated or increased in various regions, including all vulnerable regions, when c- fos mRNA had already declined to near basal levels. Compared to c- fos and c- jun, junB induction was less pronounced and confined largely to the dentate gyrus. NGFI-B mRNA increased moderately and only in brain regions exhibiting the most dramatic c- fos increases and with similar kinetics. The differential activation of the investigated IEGs suggests that rather complex long-term adaptive processes may be initiated at the genomic level after global ischemia. The present findings provide further evidence that the activation of IEGs forms part of the brain's metabolic response to ischemia, but no simple correlation appears to exist between the induction of the investigated IEGs and the phenomenon of selective vulnerability.

scholarly journals Differential Transcription and Translation of Immediate Early Genes in the Gerbil Hippocampus after Transient Global Ischemia

1993 ◽  
Vol 13 (6) ◽  
pp. 914-924 ◽  
Author(s):  
Marika Kiessling ◽  
Gabriele Stumm ◽  
Yaxia Xie ◽  
Thomas Herdegen ◽  
Adriano Aguzzi ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Glutamate Receptor ◽  
Immediate Early Genes ◽  
Immediate Early Gene ◽  
Global Ischemia ◽  
Early Gene ◽  
Immediate Early ◽  
Early Genes ◽  
Encoded Proteins ◽  
Transient Global Ischemia

Excitotoxic activation of glutamate receptors is thought to be a key event for the molecular pathogenesis of postischemic delayed neuronal death of CA-1 neurons in the gerbil hippocampus. Glutamate receptor stimulation also causes induction of transcription factors that belong to the class of immediate early genes. We examined the expression of six different immediate early genes in the gerbil hippocampus after transient global ischemia. Comparative analysis of c-fos and Krox-24 expression was carried out in the same animals at the transcriptional and translational level by in situ hybridization and immunocytochemistry. Postischemic synthesis of four additional immediate early gene (IEG)–encoded proteins (FOS-B, c-JUN, JUN-B, and JUN-D) was investigated by immunocytochemistry at recirculation intervals between 1 and 48 h. After 5 min of ischemia, transcription of c-fos and Krox-24 mRNA was induced in all hippocampal subpopulations with peak expression at 1 h after recirculation. In vulnerable CA-1 neurons, increased transcription of c-fos and Krox-24 was not followed by translation into protein. Induction of immediate early gene-encoded proteins was restricted to neuronal populations less vulnerable to brief ischemia and identified neurons that are targets of glutamate receptor-mediated neurotoxicity but that are destined to survive. Our data indicate an asynchronous synthesis and persistence of individual IEG-encoded proteins in these neurons. The staggered induction implies that combinatorial changes of transcription factors allow a differential postischemic regulation of target gene expression both spatially and over time.

Focal brain injury induces multiple immediate early genes encoding zinc finger transcription factors

1995 ◽  
Vol 28 (1) ◽  
pp. 157-163 ◽  
Author(s):  
Jari Honkaniemi ◽  
Stephen M. Sagar ◽  
Ilkka Pyykönen ◽  
Kathleen J. Hicks ◽  
Frank R. Sharp
Keyword(s):  
Transcription Factors ◽  
Brain Injury ◽  
Zinc Finger ◽  
Immediate Early Genes ◽  
Immediate Early ◽  
Early Genes ◽  
Focal Brain Injury ◽  
Genes Encoding

Activation of immediate early genes by nicotine after chronic neonatal nicotine exposure in brain areas involved in stress and anxiety responses

2018 ◽  
Vol 1687 ◽  
pp. 32-40 ◽  
Author(s):  
Amal A. Halawa ◽  
Joanne C Damborsky ◽  
G. Simona Slaton ◽  
Ursula H. Winzer-Serhan
Keyword(s):  
Immediate Early Genes ◽  
Immediate Early ◽  
Nicotine Exposure ◽  
Brain Areas ◽  
Early Genes

Intestinal perfusion induces rapid activation of immediate-early genes in weaning rats

2001 ◽  
Vol 281 (4) ◽  
pp. R1274-R1282 ◽  
Author(s):  
Lan Jiang ◽  
Heather Lawsky ◽  
Relicardo M. Coloso ◽  
Mary A. Dudley ◽  
Ronaldo P. Ferraris
Keyword(s):  
Mrna Expression ◽  
Target Genes ◽  
De Novo ◽  
Immediate Early Genes ◽  
Regulatory Elements ◽  
Intestinal Perfusion ◽  
Immediate Early ◽  
Mrna Levels ◽  
Early Genes

C- fos and c- jun are immediate-early genes (IEGs) that are rapidly expressed after a variety of stimuli. Products of these genes subsequently bind to DNA regulatory elements of target genes to modulate their transcription. In rat small intestine, IEG mRNA expression increases dramatically after refeeding following a 48-h fast. We used an in vivo intestinal perfusion model to test the hypothesis that metabolism of absorbed nutrients stimulates the expression of IEGs. Compared with those of unperfused intestines, IEG mRNA levels increased up to 11 times after intestinal perfusion for 0.3–4 h with Ringer solutions containing high (100 mM) fructose (HF), glucose (HG), or mannitol (HM). Abundance of mRNA returned to preperfusion levels after 8 h. Levels of c- fos and c- jun mRNA and proteins were modest and evenly distributed among enterocytes lining the villi of unperfused intestines. HF and HM perfusion markedly enhanced IEG mRNA expression along the entire villus axis. The perfusion-induced increase in IEG expression was inhibited by actinomycin-D. Luminal perfusion induces transient but dramatic increases in c- fos and c- jun expression in villus enterocytes. Induction does not require metabolizable or absorbable nutrients but may involve de novo gene transcription in cells along the villus.

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