Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA354945 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Neuronal activity, TGFβ signaling and unpredictable chronic stress affect transcription of Gadd45 family members in vitro and in vivo
| PRJNA354940 | ENA
Project description:Neuronal activity, TGFβ signaling and unpredictable chronic stress affect transcription of Gadd45 family members in vitro and in vivo [MeDIP-Seq]
| PRJNA354944 | ENA
Project description:Neuronal activity is altered in several neurological and psychiatric diseases. Upon depolarization not only neurotransmitters are released but also cytokines and other activators of signaling cascades. Unraveling their complex implication in transcriptional control in receiving cells will contribute to understand specific central nervous system (CNS) pathologies and will be of therapeutical interest. In this study we depolarized mature hippocampal neurons in vitro using KCl and revealed increased release not only of Brain-derived neurotrophic factor (BDNF), but also of Transforming growth factor beta (TGFB). Neuronal activity together with BDNF and TGFB controls transcription of DNA modifying enzymes specifically members of the DNA-damage-inducible (Gadd) family, Gadd45a, Gadd45b, and Gadd45g. MeDIP followed by massive parallel sequencing and transcriptome analyses revealed less DNA methylation upon KCl treatment. Thereby, psychiatric disorder-related genes, namely Tshz1, Foxn3, Jarid2, Per1, Map3k5, and Arc are transcriptionally activated and demethylated upon neuronal activation. To analyze whether misexpression of Gadd45 family members can be associated with psychiatric diseases, we applied unpredictable chronic mild stress (UCMS) as established model for depression to mice.UCMS lead to a reduced expression of Gadd45 family members. Taken together, our data demonstrate that Gadd45 family members are new putative targets for UCMS treatments.
2017-12-31 | GSE90508 | GEO
Project description:Neuronal activity is altered in several neurological and psychiatric diseases. Upon depolarization not only neurotransmitters are released but also cytokines and other activators of signaling cascades. Unraveling their complex implication in transcriptional control in receiving cells will contribute to understand specific central nervous system (CNS) pathologies and will be of therapeutical interest. In this study we depolarized mature hippocampal neurons in vitro using KCl and revealed increased release not only of Brain-derived neurotrophic factor (BDNF), but also of Transforming growth factor beta (TGFB). Neuronal activity together with BDNF and TGFB controls transcription of DNA modifying enzymes specifically members of the DNA-damage-inducible (Gadd) family, Gadd45a, Gadd45b, and Gadd45g. MeDIP followed by massive parallel sequencing and transcriptome analyses revealed less DNA methylation upon KCl treatment. Thereby, psychiatric disorder-related genes, namely Tshz1, Foxn3, Jarid2, Per1, Map3k5, and Arc are transcriptionally activated and demethylated upon neuronal activation. To analyze whether misexpression of Gadd45 family members can be associated with psychiatric diseases, we applied unpredictable chronic mild stress (UCMS) as established model for depression to mice.UCMS lead to a reduced expression of Gadd45 family members. Taken together, our data demonstrate that Gadd45 family members are new putative targets for UCMS treatments.
2017-12-31 | GSE90509 | GEO
Project description:Isogenic hESC clones with and without the FX mutation that share the same genetic background were in vitro differentiated into neurons. FX neurons present delayed neuronal development and maturation with full FMRP silencing. Following enrichment of neurons in the culture by MACS, transcriptome analysis by RNA sequencing at different time points during differentiation demonstrated dysregulation of the TGFβ/BMP signaling pathway and genes related to the extracellular matrix. FX neurons showed decreased neurite outgrowth that was rescued by inhibition of the TGFβ/BMP signaling pathway, this treatment did not affect the outgrowth of control neurons. In FMRP expressing neurons the regulation of the TGFβ/BMP pathway allow typical neurite outgrowth and axonogenesis that will eventually result in normal neuronal network activity. In contrast, in FX neurons the lack of FMRP dysregulate members of the BMP signaling pathway associated with the ECM organization that in a yet unknown mechanism, reduces the guidance of axonal growth cones, leading to an aberrant neuronal network function. Overall, our results provide new insights into the molecular pathways by which loss of FMRP affects neuronal network development which probably leads to its aberrant function in FXS.
2022-08-31 | GSE206088 | GEO
Project description:TGFβ is one of most intensively studied regulators of extracellular matrix formation, and has been implicated in the development of pulmonary fibrosis in different models. However, little is know about the role of miRNAs in TGFβ mediated fibrogenic gene regulation. By using miRNA qRT-PCR array, we have identified miRNAs whose expression are regulated by TGFβ in IMR-90 cells. Among those down-regulated miRNAs are miR-29 family members. Knockdown miR-29 in IMR-90 cells results in up-regulation of a large number of extracellular matrix and fibrogenic genes including family members of collagen, laminin, integrin, ADAM and MMP, many of them are predicted or confirmed miR-29 targets. Hierarchichal clustering analysis of mRNA array data revealed that many extracellular matrix and fibrogenic genes up-regulated by TGFβ in IMR-90 cells, are also up-regulated in miR-29 KD cells. Moreover, the similar set of extracellular matrix and fibrogenic genes is also significantly up-regulated in bleomycin treated mouse lungs. Together, our data strongly suggest that downstream of the TGFβ, miR-29 is a master modulator of genes involved in extracellular matrix formation and might play a significant role in pulmonary fibrosis.
2010-03-01 | GSE18651 | GEO
Project description:Affymetrix SNP array data for samples of 9 members of a FNMTC family
| PRJNA303172 | ENA
Project description:Gene expression was studied from the blood derived RNAs of the Finnish family members as well as from 10 controls using GeneChip Human Genome U133 Plus2 (Affymetrix). Eight out of 10 family members in the expression analysis are heterozygous for the NPAT c.2437-2438delAG, three of which are NLPHL cases.
2011-04-14 | GSE28536 | GEO
Project description:The goals of this study are to compare NGS in 3day post fertilized zebrafish embryo after knockout terfa (telomere repeats binding factor 2). In order to investigate the role of terfa in DDR, telomere protection and neuro-development. Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the zebrafish genome (build zv10) and identify 8840 NGS in 'WT vs terfa-/-' group and 4137 NGS in 'WT vs terfa+/-' group. Our results indicate that zebrafish terfa involved in 1. cell cycle dysregulation (e.g. senescence, p53, spliceosome, RNA transport, Ribosome, mRNA surveillance and cell cycles), including an increased expression of two p53-targeted genes, cdkn1a (p21) and gadd45; 2. inflammation (e.g. Salmonella and Herpes simplex infections, TOL-like receptor signaling and Cell Adhesion), including an increased expression of two pro-inflammatory genes, il6 and isg15. 3. neuronal dysfunction (e.g. Phototransduction, Calcium signaling and Neuroactive ligand-receptor interaction), including a signature of glial injury (gfap, ctsl, metrn, gcm2, clu and 5 members of the slc1a family (3, 4, 5, 7, 8)).
2022-03-09 | GSE173639 | GEO
Project description:Glioblastoma stem cells (GSCs) fate is controlled by environmental cues, among which cytokines play a crucial role. The transforming growth factor β (TGFβ) family signaling pathways controls GSCs. On one hand, TGFβ promotes cell proliferation in GBM, it induces the expression of platelet-derived growth factor-B (PDGFB). Moreover, TGFβ, via its signaling mediators Smad2/3, induces the expression of the cytokine leukemia inhibitory factor (LIF) and Sox4, which in turn enhances the expression of the stem cell transcription factor Sox2; this increases the self-renewal capacity of the GSCs and their stemness characteristics, and enhances the GSC tumor-initiating potential. On the other hand, Bone morphogenic proteins (BMPs) are known to promote GSC differentiation towards the astrocytic phenotype. To further understand which genes are regulated by TGFβ and BMP7 in GSCs we performed a microarray in the Affymetrix HTA2 platform in three different glioblastoma cell line, U2987, and two patient-derived glioblastoma stem cells, U3031MG and U3034MG, in the presence or absence of 5 ng/ml of TGFβ or 30 ng/ml BMP7 for 24 h, three biological replicates per condition.
2020-09-01 | E-MTAB-9076 | biostudies-arrayexpress