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Expression data from adult rat subventricular zone cells

ABSTRACT: Transforming growth factor (TGF)-ß1 is a multifunctional cytokine regulating a number of physiological and patho-physiological processes in the adult brain. Its expression is elevated during neurodegeneration, which is associated with reduced levels of neurogenesis. We have postulated that TGF-ß1 might be one of the crucial factors involved in limiting neurogenesis in the diseased brain. We used microarrays to detail the gene expression profile after TGFbeta-1 treatment and identified distinct classes of up- and downregulated genes. Keywords: control versus TGFbeta1 treated group

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE14556 | GEO | 2011/05/10

SECONDARY ACCESSION(S): PRJNA111735

REPOSITORIES: GEO

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Expression data from adult rat subventricular zone cells

Project description:Transforming growth factor (TGF)-ß1 is a multifunctional cytokine regulating a number of physiological and patho-physiological processes in the adult brain. Its expression is elevated during neurodegeneration, which is associated with reduced levels of neurogenesis. We have postulated that TGF-ß1 might be one of the crucial factors involved in limiting neurogenesis in the diseased brain. We used microarrays to detail the gene expression profile after TGFbeta-1 treatment and identified distinct classes of up- and downregulated genes. Keywords: control versus TGFbeta1 treated group Adult rat subventricular zone cells were cultured for 7 days under proliferation conditions. Control cells were exposed to HCl/BSA whereas TGFbeta-1 treated cells received 10 ng/ml TGFbeta-1 dissolved in HCl/BSA 3 times per week. RNA was extracted followed by hybridization on Affymetrix microarrays.

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Expression data from adult rat subventricular zone cells

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Expression data from adult rat subventricular zone cells

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Structural determinants of heparin–transforming growth factor-β1 interactions and their effects on signalling

Project description:Transforming growth factor-ß1 (TGF-ß1, Uniprot: P01137) is a heparin-binding protein that has been implicated in a number of physiological processes, including the initiation of chondrogenesis by human mesenchymal stem cells (hMSCs). Here, we identify the molecular features in the protein and in heparin required for binding and their effects on the potentiation of TGF-ß1’s activity on hMSCs. Using a proteomics “Protect and Label” approach, lysines K291, K304, K309, K315, K338, K373, K375 and K388 were identified as being directly involved in binding heparin. Competition assays in an optical biosensor demonstrated that TGF-ß1 does require N- and 6-O-sulfate groups for binding but that 2-O-sulfate groups are unlikely to underpin the interaction. Heparin-derived oligosaccharides as short as degree of polymerization (dp) 4 have a weak ability to compete for TGF-ß1 binding to heparin, which increases with the length of the oligosaccharide to reach a maximum between dp18 and dp24. In cell-based assays, heparin, 2-O-, 6-O- and N-desulfated re-N-acetylated heparin and oligosaccharides 14–24 saccharides (dp14–24) in length all increased the phosphorylation of SMAD2 after 6 h of stimulation with TGF-ß1. The results provide the structural basis for a model of heparin/heparan sulfate binding to TGF-ß1 and demonstrate that the features in the polysaccharide required for binding are not identical to those required for sustaining the signaling by TGF-ß1 in hMSCs.

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Systematic investigation of cytokine signaling activity at the tissue and single-cell levels

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Effect of simultaneous activation of TGFbeta and TLR4 pathway in human monocytes

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2006-12-31 | E-MEXP-566 | biostudies-arrayexpress

Primary and ras keratinocytes plus TGFbeta1

Project description:We have compared the response to TGFbeta1 in normal and v-rasHa transduced primary mouse keratinocytes using NCI cDNA microarrays. This analysis reveals that Ha-ras alters global TGFbeta1 mediated gene expression in a gene specific manner. The expression pattern of TGFbeta1 immediate early response genes and down regulation of cell cycle control genes is not altered by Ha-ras but the induction of most extracellular matrix genes is blocked. Using Smad3 null keratinocytes, we find that the majority of TGFbeta1 responsive genes in primary keratinocytes are Smad3 dependent, but patterns of transcriptional responses suggest that the ability of Ha-ras to block TGFbeta1 mediated gene expression is not dependent on Smad3. However, the combination of oncogenic ras and loss of Smad3 prevents the TGFbeta1 dependent suppression of genes associated with cell cycle progression and apoptosis observed with either genotype alone. In addition several extracellular matrix genes are super-repressed by TGFbeta1 in the Ha-ras Smad3 null keratinocytes. These data provide a genomic framework for understanding how disruptions of TGFbeta signaling and oncogenic ras cooperate to promote premalignant progression of primary keratinocytes. Keywords: time series design

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TGFbeta lung fibroblasts

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Molecular characterization of adult mouse subventricular zone progenitor cells during the onset of differentiation

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