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Effect of acute and chronic social stress on hippocampal transcriptome in mice.

ABSTRACT: We investigated gene expression in mice subjected to acute and chronic social stress of different duration. Microarray data showed that chronic stress affected genes involved in function of vascular system (Alas2, Hbb-b1, Hba-a2, Hba-a1), injury response (Vwf, Mgp, Cfh, Fbln5, Col3a1, Ctgf) and inflammation (Isg20, Ctla2a, Ctla2b,Lcn2, Lrg1, Rsad2,S100a8, S100a9). Review of the literature revealed that the most frequently regulated genes (up or down) were Igfbp2, Igf2, Prlr, App, Cdh1, Col1A1, Clic6, Enpp2, Sostdc1,Itgb6, Mef2c, Spp1, and Zeb2. Obtained results suggest that stress may affect brain functions through the stress-induced dysfunction of the vascular system. Some of the key genes revealed by the review of published data participate both in the response to injury and in the mechanism of learning and memory. These genes may constitute a link between stress and stress-induced memory impairments. An important issue raised by our work is also the risk of tissue contamination with choroid plexus. Such contamination would result in consistent up- or down-regulation of genes, such as Ttr, Igf2, Igfbp2, Prlr, Enpp2, Sostdc1, 1500015O10RIK (Ecrg4), Kl, Clic6, Kcne2, F5, Slc4a5, and Aqp1. The study was supported by Grant N N311 604938, 2011/03/N/NZ29/05222 and partially by IP2011 030371. Statistical analysis of microarray data was supported with Grant N N519 657940.

ORGANISM(S): Mus musculus

PROVIDER: GSE59070 | GEO | 2014/07/04

SECONDARY ACCESSION(S): PRJNA254338

REPOSITORIES: GEO

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Effect of acute and chronic social stress on hippocampal transcriptome in mice.

Project description:We investigated gene expression in mice subjected to acute and chronic social stress of different duration. Microarray data showed that chronic stress affected genes involved in function of vascular system (Alas2, Hbb-b1, Hba-a2, Hba-a1), injury response (Vwf, Mgp, Cfh, Fbln5, Col3a1, Ctgf) and inflammation (Isg20, Ctla2a, Ctla2b,Lcn2, Lrg1, Rsad2,S100a8, S100a9). Review of the literature revealed that the most frequently regulated genes (up or down) were Igfbp2, Igf2, Prlr, App, Cdh1, Col1A1, Clic6, Enpp2, Sostdc1,Itgb6, Mef2c, Spp1, and Zeb2. Obtained results suggest that stress may affect brain functions through the stress-induced dysfunction of the vascular system. Some of the key genes revealed by the review of published data participate both in the response to injury and in the mechanism of learning and memory. These genes may constitute a link between stress and stress-induced memory impairments. An important issue raised by our work is also the risk of tissue contamination with choroid plexus. Such contamination would result in consistent up- or down-regulation of genes, such as Ttr, Igf2, Igfbp2, Prlr, Enpp2, Sostdc1, 1500015O10RIK (Ecrg4), Kl, Clic6, Kcne2, F5, Slc4a5, and Aqp1. This is analysis of 24 hippocampal RNA samples. Each sample consisted of equal amounts of total RNA from 3 mice subjected to the same experimental condition. Comparisons: acute stress vs. acute control (unstressed), stress-8 days vs. control-8 days, stress-13 days vs. control-13 days, stress-13 days+5 days of rest vs. control-13 days+5 days of rest. 3 biological replicates in each comparison. Dye swap (technical replicate) was included for each biological replicate.

2014-07-04 | E-GEOD-59070 | biostudies-arrayexpress

A distinct subpopulation of follicular helper T (Tfh) cells promotes Tfr cell differentiation by producing Sostdc1

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Project description:Transcriptional effects in circulating leukocytes from mice challenged to peritoneal contamination and infection (PCI) compared to sham (vehicle control). We gratefully acknowledge the BMBF grant for the Center for Sepsis Control and Care (CSCC) for this study

2017-09-01 | GSE36608 | GEO

IGF2 mRNA Binding Protein-2 is a tumor promoter that drives cancer proliferation through its client mRNAs IGF2 and HMGA1

Project description:The gene encoding the IGF2 mRNA binding protein-2/IMP2 is amplified and overexpressed in many cancers, accompanied by a poorer prognosis. Mice deficient in IMP2 exhibit a longer lifespan and a reduced tumor burden at old age. Herein we show in a diverse array of cancer cells that IMP2 overexpression stimulates and IMP2 elimination diminishes proliferation by 50-80%. In addition to its known ability to promote IGF2 abundance, we find that IMP2 strongly promotes IGF action, by binding and stabilizing HMGA1 mRNA. The HMGA1 DNA binding protein, a known oncogene, suppresses the abundance of IGFBP2 and Grb14, inhibitors of IGF action. IMP2 stabilization of HMGA1 mRNA plus IMP2 stimulated IGF2 production synergistically drive cancer cell proliferation and account for IMP2’s tumor promoting action. IMP2’s ability to promote proliferation and IGF action requires mTOR-catalyzed IMP2 phosphorylation.

2017-09-14 | GSE101311 | GEO

ChIP-Chip tiling array for H3k27ac in mouse β-TC3 cells over panel of genes including Pax6, Sox2, Otx2, Sox9.

Project description:Enhancer identification using H3k27ac ChIP-ChIP in mouse β-TC3 cells, using custom tilling array covering a 66 Mb region around Pax6 (Chr2:75,000,000-141,000,000) mm9. Additional loci and regions, Sox2 (chr3:32,000,000-37,000,000), Otx2 (chr14:48,500,000-50,500,000), Rax (chr18:65,500,000-68,000,000), Hba a-globin (chr11:32,050,000-32,450,000), Six3 (chr17:85,200,000-86,700,000), Sox1 (chr8:11,800,000-12,800,000), Mab21L2 (chr3:85,850,000-86,850,000), Bmp4 (chr14:46,500,000-47,500,000), NeuroD1 (chr2:79,050,000-79,600,000), Prox1 (chr1:191,700,000-192,700,000), Hmx1 (chr5:34,700,000-36,200,000), H19-Igf2 (chr7:149500000-150500000), Sox9 (chr11:110000000-116000000).

2018-08-01 | GSE116805 | GEO

ChIP-Chip tiling array for H3k27ac in mouse MV+ (lens epithelium) and RAG cells ( renal adenocarcinoma) over panel of genes including Pax6, Sox2, Otx2, Sox9.

Project description:Enhancer identification using H3k27ac ChIP-ChIP in mouse MV+ and RAG, using custom tilling array covering a 66 Mb region around Pax6 (Chr2:75,000,000-141,000,000) mm9. Additional loci and regions, Sox2 (chr3:32,000,000-37,000,000), Otx2 (chr14:48,500,000-50,500,000), Rax (chr18:65,500,000-68,000,000), Hba a-globin (chr11:32,050,000-32,450,000), Six3 (chr17:85,200,000-86,700,000), Sox1 (chr8:11,800,000-12,800,000), Mab21L2 (chr3:85,850,000-86,850,000), Bmp4 (chr14:46,500,000-47,500,000), NeuroD1 (chr2:79,050,000-79,600,000), Prox1 (chr1:191,700,000-192,700,000), Hmx1 (chr5:34,700,000-36,200,000), H19-Igf2 (chr7:149500000-150500000), Sox9 (chr11:110000000-116000000).

2018-10-18 | GSE119659 | GEO

Sost and its paralog Sostdc1 coordinate digit number in a Gli3-dependent manner

Project description:WNT signaling is critical in most aspects of skeletal development and homeostasis, and antagonists of WNT signaling are emergning as key regulatory proteins with great promise as therapeutic agents for bone disorders. Until recently Sost and its paralog Sostdc1 have been described as growth factors with highly restricted expression in the adult where Sost was assumed 'osteocyte-' and Sostdc1 'kidney-' specific. Here we show that these two proteins emerged throgh ancestral genome duplication and their expression patterns have diverged to span complimentary domains in most organ systems including musculoskeletal, cardiovascular, nervous, digestive, reproductive and respiratory. In the developing limb, Sost and Sostdc1 display dynamic expression patterns with Sost being restricted to the distal ectoderm and Sostdc1 to the proximal ectoderm and the mesenchyme. While Sostdc1-/- mice lack any obvious limb and skeletal defects, Sost-/- mice recapitulate the hand defects described for sclerosteosis patients. However, elevated WNT signaling in Sost-/-; Sostdc1-/- mice causes misregulation of SHH signaling, ectopic activation of Sox9 in the digit 1 field and ultimately preaxial polydactyly. In addition, we show that the syndactyly documented in Sclerosteosis is present in both Sost-/- and Sost-/-; Sostdc1-/- mice, and is driven by misregulation of Fgf8 in the AER, a region lacking Sost and Sostdc1 expression. This study highlights the complexity of WNT signaling in skeletal biology and disease and emphasizes how redundant mechanisms and non-cell autonomous effects can synergize to unveil new intricate phenotypes caused by elevated WNT signaling.

2013-08-17 | GSE44325 | GEO

ChIP-Chip tiling array for CTCF and Rad21 in mouse β-TC3 cells (pancreatic insulinoma) MV+ (lens epithelium) and RAG cells (renal adenocarcinoma) over panel of genes including Pax6, Sox2, Otx2, Sox9.

Project description:CTCF and Rad21 ChIP-ChIP in mouse pancretic cells, pancreatic β-TC3 cells, lens epithelium MV+ cells and renal adenocarcinoma RAG cells, using custom tilling array covering a 66 Mb region around Pax6 (Chr2:75,000,000-141,000,000) mm9. Additional loci and regions, Sox2 (chr3:32,000,000-37,000,000), Otx2 (chr14:48,500,000-50,500,000), Rax (chr18:65,500,000-68,000,000), Hba a-globin (chr11:32,050,000-32,450,000), Six3 (chr17:85,200,000-86,700,000), Sox1 (chr8:11,800,000-12,800,000), Mab21L2 (chr3:85,850,000-86,850,000), Bmp4 (chr14:46,500,000-47,500,000), NeuroD1 (chr2:79,050,000-79,600,000), Prox1 (chr1:191,700,000-192,700,000), Hmx1 (chr5:34,700,000-36,200,000), H19-Igf2 (chr7:149500000-150500000), Sox9 (chr11:110000000-116000000).

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2020-08-25 | GSE156774 | GEO

Translation in human mature erythrocytes

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2023-03-10 | PXD021774 | Pride

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