| Abstract No.: | A-B1040 |
| Country: | Canada |
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| Title: | THE INDUCTION OF EARLY GROWTH RESPONSE 2 (EGR 2) IS TRIGGERED BY NEURONAL ACTIVITY-DEPENDENT NF-KB ACTIVATION
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| Authors/Affiliations: | 1 Solmaz Nafez*; 1 Kensuke Oikawa; 1 Gary Odero; 2 Michael Sproule; 1 Ning Ge; 1 Dali Zhang; 1 Bernard Abrenica; 1 Michael Czubryt; 1 Benedict Albensi;
1 University of Manitoba, Winnipeg,MB, Canada; 2 University of Winnipeg, MB, Canada
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| Content: | Objective: NF-κB mediated signaling is complex and plays a critical role in many biological processes. Investigators have reported that NF-κB is activated during the induction of long term potentiation (LTP) and may be a requirement for synaptic plasticity and memory. In an attempt to explore target genes of NF-kB in LTP, we identified early growth response 2 (Egr 2) as one of targets of NF-kB. The present study focused on obtaining evidence of the linkage between the induction of Egr 2 and NF-kB signaling pathway.
Materials and Methods: We analyzed transcriptomes of LTP-induced hippocampal slices (CA1 region) from 2-month-old NF-kB p50 knockout mice (p50-/-) versus its littermate (p50+/+) to identify target genes of NF-kB. LTP was evoked by applying theta-burst stimulation to Schaffer collateral axon in the CA1 region. At 3hr after conditioning, total mRNA samples were extracted from LTP-induced slices and non-stimulated control slices. These mRNA samples were subjected to the DNA microarray analysis (Affymetrix GeneChip® Mouse Genome 430 2.0) and real-time RT-qPCR. We also examined the mRNA and protein expression level of Egr 2 in HeLa cells using real-time RT-qPCR and Western blotting. TNF α was used for activating NF-kB signaling pathway in HeLa cells. The P-Match software was used for sequence analysis of distal promoter region of Egr 2. [Results] There were no significant differences of both basal synaptic transmission and LTP magnitude in p50 -/- and p50 +/+. We identified early growth response 2 (Egr2) is inducted by NF-kB activation during LTP. From the gene-structure analysis, we found several NF-kB consensus binding sites around promoter region of Egr2. In addition, the upregulation of Egr2 mRNA in HeLa cells treated with TNFα, an activator of the NF-kB signaling pathway, has been observed.
Conclusion: These data suggest that Egr2 expression level is controlled by direct transcriptional activity of NF-kB.
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