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The role of Egr1 and FosB in the 6 hour injury response

ABSTRACT: This trancriptome analysis reports genes that are differentially expressed in wildtype (WT) lens epithelial cells (LEC) between 6 hours and zero hours after injury, and between Egr1 (E1) or FosB (FB) null LEC and wildtype LEC at zero hours (0H) and at 6 hours (6H) after injury.

ORGANISM(S): Mus

PROVIDER: GSE206574 | GEO | 2022/11/16

REPOSITORIES: GEO

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The six-hour injury response in lens epithelial cells

Project description:This trancriptome analysis reports genes that are differentially expressed in wildtype (WT) lens epithelial cells (LEC) between 6 hours and zero hours after injury.

2022-11-16 | GSE206563 | GEO

The role of Egr1 and FosB in the 6 hour injury response

Project description:The role of Egr1 and FosB in the 6 hour injury response

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Expression data from fosb gene modified mouse

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Expression data from fosb gene modified mouse

Project description:To examine fosB regulation of neurogenesis, depression and epilepsy, we compared the gene expression profiles of wild type, fosBd/d and fosB-null mice by microarray analysis. Microarray analysis revealed that genes related to neurogenesis, depression and epilepsy are altered in the hippocampus of fosB-null mice. Total RNA from the hippocampus of wild-type, fosBd/d and fosB-null mice was prepared using ISOGEN and RNeasy Mini kits. For DNA microarray experiments, total RNA (100ng) was added to poly-A control and treated with WT Expression Kit. cDNA was labeled using WT terminal labeling kit and hybridized with Affymetrix GeneChip Mouse Gene 1.0 ST platform (GPL6246).

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Fosb gene products contribute to excitotoxic microglial activation by regulating the expression of complement C5a receptors in microglia

Project description:The Fosb gene encodes subunits of the activator protein-1 transcription factor complex. Two mature mRNAs, Fosb and ΔFosb, encoding full-length FOSB and ΔFOSB proteins respectively, are formed by alternative splicing of Fosb mRNA. Fosb products are expressed in several brain regions. Moreover, Fosb-null mice exhibit depressive-like behaviors and adult-onset spontaneous epilepsy, demonstrating important roles in neurological and psychiatric disorders. Study of Fosb products has focused almost exclusively on neurons; their function in glial cells remains to be explored. In this study, we found that microglia express equivalent levels of Fosb and ΔFosb mRNAs to hippocampal neurons and, using microarray analysis, we identified six microglial genes whose expression is dependent on Fosb products. Of these genes, we focused on C5ar1 and C5ar2, which encode receptors for complement C5a. In isolated Fosb-null microglia, chemotactic responsiveness toward the truncated form of C5a was significantly lower than that in wild-type cells. Fosb-null mice were significantly resistant to kainate-induced seizures compared with wild-type mice. C5ar1 mRNA levels and C5aR1 immunoreactivity were increased in wild-type hippocampus 24 hours after kainate administration; however, such induction was significantly reduced in Fosb-null hippocampus. Furthermore, microglial activation after kainate administration was significantly diminished in Fosb-null hippocampus, as shown by significant reductions in CD68 immunoreactivity, morphological change and reduced levels of Il6 and Tnf mRNAs, although no change in the number of Iba-1-positive cells was observed. These findings demonstrate that, under excitotoxicity, Fosb products contribute to a neuroinflammatory response in the hippocampus through regulation of microglial C5ar1 and C5ar2 expression.

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Expression data from primary cultured microglia from Fosb-null mouse

Project description:To identify genes whose expression is regulated by Fosb gene products in microglia, we performed microarray analysis using RNA prepared from wild-type and fosB-null microglial cells. Microarray analysis revealed that expression levels of 6 genes are altered in primary cultured microglial cells prepared from fosB-null mice compared with wild type. fosB+/G mice with a null-mutant allele, fosBG, were established and maintained by backcrossing to C57BL/6J. To yield homozygous mutant mice, fosB+/G (N20 generation) mice were intercrossed. C57BL/6J mice were used as wild-type control.

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Development of gene expression signatures for the A549 cells that overexpressed of FOSB

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FosB-regulated gene expression in venral hippocampo-accumbal projection neurons

Project description:We examined here the regulation of gene expression in ventral hippocampus neurons that project to nucleus accumbens (vHPC-NAc) by the transcription factor, ΔFosB. The activity of this circuit is critical to stress-induced social withdrawal. ΔFosB regulates the physiology and behavior of this circuit to produce resilience. Circuit-specific translating ribosomal affinity purification (TRAP) was conducted followed by RNASeq. A strain of floxed Fosb mice (the gene that encodes ΔFosB) was crossed with a ribosomal L10-GFP fusion protein line (Rosa26). To target vHPC-NAc neurons, a retrograde recombinant HSV-Cre was injected into NAc to retrogradely drive expression of GFP and knockout the Fosb gene in vHPC-NAc. Bilateral biopsy punches of vHPC containing GFP-labeled projections were collected, pooled, and processed by TRAP followed by 3rd-generation sequencing of actively translating mRNA. We have now identified Fosb-regulated gene expression in a specific hippocampal-to-accumbens circuit that is important for resilience to stress-induced social withdrawal.

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Gene-targeted, CREB-mediated induction of ∆FosB controls distinct downstream transcriptional patterns within D1 and D2 medium spiny neurons

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Pitx2 maintains mitochondrial function during regeneration to prevent myocardial fat deposition

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