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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Imprinting RNAseq

ABSTRACT: Long-term hematopoietic stem cells (HSCs), short-term HSCs and multipotent progenitor cells (MPPs) were isolated from bone marrow of four mouse strains (WT, H19-deletion, Igf1r-deletion, and double-deletion) and expression profiled with RNAseq. The behavior of the transcriptomes, and in particular the imprinted genes, was analyzed to see what might be involved in maintaining quiescence of long-term stem cells, and how H19 and Igf1r affected the expression of imprinted genes. Transcriptional profiling data of the same cells have been deposited in ArrayExpress under accession number E-MTAB-1644 (http://wwwdev.ebi.ac.uk/arrayexpress/experiments/E-MTAB-1644/).

INSTRUMENT(S): Illumina HiSeq 2000

ORGANISM(S): Mus musculus

SUBMITTER: Ariel Paulson

PROVIDER: E-MTAB-1628 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Maternal imprinting at the H19-Igf2 locus maintains adult haematopoietic stem cell quiescence.

Venkatraman Aparna A He Xi C XC Thorvaldsen Joanne L JL Sugimura Ryohichi R Perry John M JM Tao Fang F Zhao Meng M Christenson Matthew K MK Sanchez Rebeca R Yu Jaclyn Y JY Peng Lai L Haug Jeffrey S JS Paulson Ariel A Li Hua H Zhong Xiao-bo XB Clemens Thomas L TL Bartolomei Marisa S MS Li Linheng L

Nature 20130717 7462

The epigenetic regulation of imprinted genes by monoallelic DNA methylation of either maternal or paternal alleles is critical for embryonic growth and development. Imprinted genes were recently shown to be expressed in mammalian adult stem cells to support self-renewal of neural and lung stem cells; however, a role for imprinting per se in adult stem cells remains elusive. Here we show upregulation of growth-restricting imprinted genes, including in the H19-Igf2 locus, in long-term haematopoiet ...[more]

PMID: 23863936

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Imprinting Affy

Project description:Murine long-term hematopoietic stem cells (HSCs), short-term HSCs and multipotent progenitor cells (MPPs) were isolated from bone marrow and expression profiled on Affy chips. The behavior of maternal-specific imprinting genes, particularly in the H19-Igf2 locus, was focused on, to see if any might be involved in maintaining quiescence of long-term stem cells.

2013-08-12 | E-MTAB-1644 | biostudies-arrayexpress

Protein Identification and Post-translational Analysis of DMD and its associated Proteins in H19-proficient and -deficient Cells

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Project description:Long noncoding RNAs (lncRNAs) are non-protein coding RNAs regulating gene expression. Although for some lncRNAs a relevant role in hypoxic endothelium has been shown, the regulation and function of lncRNAs is still largely unknown in the vascular physio-pathology. Taking advantage of next-generation sequencing techniques, transcriptomic changes induced by endothelial cell exposure to hypoxia were investigated. Paired-end sequencing of polyadenylated RNA derived from human umbilical vein endothelial cells (HUVECs) exposed to 1% O2 or normoxia was performed. Bioinformatics analysis identified â 2000 differentially expressed genes, including 122 lncRNAs. Extensive validation was performed by both microarray and qPCR. Among the validated lncRNAs, H19, MIR210HG, MEG9, MALAT1 and MIR22HG were also induced in a mouse model of hindlimb ischemia. To test the functional relevance of lncRNAs in endothelial cells, knockdown of H19 expression was performed. H19 inhibition decreased HUVEC growth, inducing their accumulation in G1 phase of the cell cycle; accordingly, p21 (CDKN1A) expression was increased. Additionally, H19 knockdown also diminished HUVEC ability to form capillary like structures when plated on matrigel. In conclusion, a high-confidence signature of lncRNAs modulated by hypoxia in HUVEC was identified and a significant impact of H19 lncRNA was shown. For H19 knock-down, 50 nM of antisense LNAâ¢ GapmeRs customer-designed for H19 or Negative control A (Exiqon) were transfected by siRNA transfection reagent (Santa Cruz Biotechnology) in 40% confluent HAOEC according to the manufacturerâs manual.

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Mis-expression of Igf2 and H19 work independently on distinct cell types to cause cardiomyopathy in a Beckwtih Wiedemann mouse model

Project description:Igf2 and H19 are linked, reciprocally imprinted genes that play critical roles in mammalian development. Igf2 encodes a peptide hormone, Insulin-like Growth Factor 2, that binds to the InsR and Igf1R receptor kinases to regulate cell growth and metabolism through well-established pathways. H19 encodes a 2.3 kb lncRNA whose biochemical actions are only now being identified. Here we use a mouse model to investigate cardiomyopathies associated with maternal loss of imprinting at the locus. Increased circulating levels of IGF2 during fetal development result in activation of pAKT/mTOR signaling in cardiomyocytes to cause cellular hypertrophy and hyperplasia in neonatal hearts. This neonatal hypertrophy is unaffected by H19 RNA levels. However, loss of H19 does cause fibrosis and progressive cardiac pathology in adult mice. In hearts, H19 expression is concentrated in endothelial cells associated with blood vessels and capillaries and loss of H19 results in high incidence of trans differentiation of these cells to smooth muscle. H19 encoded miRNAs 675-3p and -5p are not sufficient to promote normal development. Thus these experiments define a novel role for the H19 lncRNA in regulating cell fate.

2020-03-01 | GSE111418 | GEO

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Project description:Sequencing and analysis of hematopoietic progenitors and lineage cells, small RNA

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2014-01-22 | E-GEOD-53742 | biostudies-arrayexpress

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