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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The histone lysine demethylase Kdm6b is required for activity-dependent preconditioning of hippocampal neuronal survival

ABSTRACT: We profiled basal and bicuculline+4-AP inducible mRNA expression in cultured mouse hippocampal neurons with or without viral shRNA mediated knockdown of Kdm6b We harvested mRNA from neurons under four conditions (pLKO vector/treatment control, pLKO vector/3hr bicuculline+4AP, Kdm6b knockdown/treatment control,Kdm6b knockdown/3hr bicuculline+4AP). Libraries were generated and used for RNA sequencing.

ORGANISM(S): Mus musculus

SUBMITTER: Christopher Frank

PROVIDER: E-GEOD-58398 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The histone lysine demethylase Kdm6b is required for activity-dependent preconditioning of hippocampal neuronal survival.

Wijayatunge Ranjula R Chen Liang-Fu LF Cha Young May YM Zannas Anthony S AS Frank Christopher L CL West Anne E AE

Molecular and cellular neurosciences 20140628

Enzymes that regulate histone lysine methylation play important roles in neuronal differentiation, but little is known about their contributions to activity-regulated gene transcription in differentiated neurons. We characterized activity-regulated expression of lysine demethylases and lysine methyltransferases in the hippocampus of adult male mice following pilocarpine-induced seizure. Pilocarpine drove a 20-fold increase in mRNA encoding the histone H3 lysine 27-specific demethylase Kdm6b sele ...[more]

PMID: 24983519

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The histone lysine demethylase Kdm6b is required for activity-dependent preconditioning of hippocampal neuronal survival

Project description:We profiled basal and bicuculline+4-AP inducible mRNA expression in cultured mouse hippocampal neurons with or without viral shRNA mediated knockdown of Kdm6b

2014-06-12 | GSE58398 | GEO

Identification of response genes upon neuronal activation in mouse cortical neurons

Project description:We search for developmental changes specific to humans by examining gene expression profiles in the human, chimpanzee and rhesus macaque prefrontal and cerebellar cortex. In both brain regions, developmental patterns were more evolved in humans than in chimpanzees. The major human specific genes in prefrontal cortex was enriched in neuronal functions and regulated by several transcription factors, which were previously implicated in regulation of neuronal functions. To confirm neuronal function of the human prefrontal cortex specific genes, we identifed response genes upon neuronal activation in mouse cortical neurons. Our results show that human specific genes are enriched in the response genes upon neuronal activation, implying the function of human prefrontal cortex specific genes in synaptic development. The cortical neurons from E15 mouse were isolated and cultured. We then exposed neurons to bicuculline (Bic), or potassium chloride (KCl), or without treatment. The cultured neurons under each group were hybridized to Agilent whole mouse genome oligo microarray (4x44k).

2012-02-02 | E-GEOD-29139 | biostudies-arrayexpress

A comparative transcriptomics approach unveils networks of activity-driven neuronal gene expression

Project description:Primary cultured hippocampal neurons were infected with lentiviral particles bearing constitutively active versions of the transcription factors CREB, SRF, EGR1 and FOS to define the downstream genetic program associated with each of these paradigmatic transcription factors in neurons. For CREB, we also extracted samples at a shorter infection time to try to dissect the different components of the wider genetic response observed upon expression of a constitutively active version of this transcription factor. In order to further explore the contribution of these transcriptional regulators to activity-driven gene expression, we also treated cultured hippocampal neurons infected with GFP-only expressing lentiviral particles with different drugs (bicuculline, forskokine, and BDNF) and profiled the associated transcriptional response. Finally, in order to further explore the role of CREB in forskolin-mediated gene expression, we also used A-CREB, a dominant negative form of this transcription factor. Specifically, we stimulated neurons with forskolin in the presence or absence of lentiviral particles expressing A-CREB and carried out genome-wide transcriptional profiling.

2011-11-19 | E-MEXP-3167 | biostudies-arrayexpress

CRISPR-Cas9 combinatorial KO of epigenetic regulators in human ovarian cancer cells

Project description:We sequenced polyA mRNA from OVCAR8-ADR-Cas9 cells in which one or two of 3 epigenetic regulators (BRD4, KDM4C, KDM6B) had been knocked out to examine how global gene expression was affected and evaluate potential synergistic effects at a molecular level. Gene expression data (RNA-Seq) in OVCAR8-ADR-Cas9 cells infected with control vector or vectors expressing gRNAs targeting one of 4 epigenetic regulators (BRD4, KDM4C, KDM6B) with biological replicates.

2015-12-17 | E-GEOD-71074 | biostudies-arrayexpress

RNA-seq analysis of bronchosphere cultures of primary human bronchiolar epithelial cells

Project description:Primary human bronchial epithelial cells were transduced with control or hYAP(S127A) lentivirus in sphere forming conditions. Bronchospheres were harvested on day 18-20 for RNAseq analysis Passage 1 Primary HBECs from 2 independent donors were transduced with control or hYAP lentivirus. 48 hours post infection, cells were plated on transwell inserts in a 50-50 mixture of ALI medium-Cultrex BME reduced growth factor (RGF) to form spheres. Well differentiated bronchospheres were harvested for RNA-seq analysis on day 18-20 by combining 3 wells of each group for each donor.

2015-01-01 | E-GEOD-61626 | biostudies-arrayexpress

Transcription profiling of mouse hippocampal slices after NMDA or forskolin-rolipram-0 Mg2+ or bicuculline treatment

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2008-06-01 | E-MEXP-1184 | biostudies-arrayexpress

KDM4B- and KDM6B-regulated genes in human mesenchymal stem cell osteogenic differentiation

Project description:To investigate how histone demethylases KDM4B and KDM6B may be involved in osteogenic commitment of mesenchymal stem cells (MSCs), we performed gene expression profiling and comparison on control, KDM4B- and KDM6B-knockdown MSCs at different stages of osteogenic differentiation. Human MSCs infected with scramble shRNAs, shRNAs against KDM4B or KDM6B are treated with BMP4/7 for 0, 4 and 24hrs. Total RNA were extracted from these 9 samples.

2012-07-31 | E-GEOD-36970 | biostudies-arrayexpress

Loss of histone demethylase KDM6B enhances aggressiveness of pancreatic cancer through downregulation of C/EBPα

Project description:Genetic mutations in pancreatic ductal adenocarcinoma (PDAC) with critical roles have been well examined. The recent discovery of alterations in genes encoding histone modifiers suggests their possible roles in the complexity of cancer development. We previously reported loss of heterozygosity of the KDM6B gene, which encodes a histone demethylase for trimethylated histone H3 lysine 27 (H3K27me3), a repressive chromatin mark, in PDAC cells. In this study, we demonstrated that loss of KDM6B enhanced aggressiveness of PDAC cells. KDM6B has been regarded as a tumor suppressor that mediates oncogenic KRAS-induced senescence. Consistently, KDM6B was highly expressed in pancreatic precancerous lesions (pancreatic intraepithelial neoplasms); then, the expression decreased as the malignant grade progressed. We found that knockdown of KDM6B in PDAC cells promoted tumor sphere formation and increased peritoneal dissemination and liver metastasis in vivo. Microarray and chromatin immunoprecipitation analysis implicated CEBPA for aggressiveness induced by KDM6B knockdown. CEBPA knockdown recapitulated the phenotypic change of PDAC cells after KDM6B knockdown, which was reversed by forced expression of C/EBPα. Moreover, similar protein expression patterns of KDM6B and C/EBPα in human PDAC emphasized their functional correlation. Notably, pharmacological inhibition of the H3K27 methylase EZH2 in PDAC cells inhibited tumor sphere formation along with the upregulation of CEBPA expression, and this effect was impaired in KDM6B knockdown cells, highlighting the role for KDM6B in the activation of CEBPA. Together, our results propose a significant role for the KDM6B-C/EBPα axis in the PDAC phenotype.

2014-06-30 | GSE28155 | GEO

Cytotoxic effects of Bortezomib in Myelodysplastic syndrome/Acute Myeloid Leukemia depend on autophagy-mediated lysosomal degradation of TRAF6 and repression of PSMA1

Project description:Bortezomib (VelcadeM-BM-)) is widely used for the treatment of various human cancers, however, its mechanisms of action are not fully understood, particularly in myeloid malignancies. Bortezomib is a selective and reversible inhibitor of the proteasome. Paradoxically, we find that Bortezomib induces proteasome-independent degradation of TRAF6 protein, but not mRNA, in Myelodysplastic syndrome (MDS) and Acute Myeloid Leukemia (AML) cell lines and primary cells. The reduction in TRAF6 protein coincides with Bortezomib-induced autophagy, and subsequently with apoptosis in MDS/AML cells. RNAi-mediated knockdown of TRAF6 sensitized Bortezomib-sensitive and -resistant cell lines, underscoring the importance of TRAF6 in Bortezomib-induced cytotoxicity. Bortezomib-resistant cells expressing an shRNA targeting TRAF6 were resensitized to the cytotoxic effects of Bortezomib due to down-regulation of the proteasomal subunit alpha-1 (PSMA1). To uncover the molecular consequences following loss of TRAF6 in MDS/AML cells, we applied gene expression profiling and identified an apoptosis gene signature. Knockdown of TRAF6 in MDS/AML cell lines or patient samples resulted in rapid apoptosis and impaired malignant hematopoietic stem/progenitor function. In summary, we describe novel mechanisms by which TRAF6 is regulated through Bortezomib/autophagy-mediated degradation and by which it alters MDS/AML sensitivity to Bortezomib by controlling PSMA1 expression. TF-1 cells were transduced with lentivirus encoding shRNA targeting human TRAF6 and a negative control (pLKO) for 2.5 days. GFP positive cells were sorted for RNA exctration, labeling, and hybridization. A total of four samples were included, and two groups are assigned. Two replicates are for each group. Comparison comprises mRNA expression profile of TRAF6 knockdown (shT6) v.s. control vector (pLKO).

2012-06-14 | E-GEOD-38519 | biostudies-arrayexpress

Functional analysis of chicken IRF7 in response to dsRNA analog poly(I:C) by integrating overexpression and knockdown

Project description:In this study, an integrative high-throughput functional genomics approach was applied by combining overexpression and knockdown assays with RNA-seq; this side-by-side approach was taken in an effort to obtain corroboration and complementary support in the identification of potential genes that are under the control of IRF7. Transcriptiome analysis of Poly(I:C) induced IRF7 overexpression & knockdown DF-1 cell lines and their respective controls

2015-06-25 | E-GEOD-70105 | biostudies-arrayexpress

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