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    Transcriptional profiling of macrophages derived from monocytes and iPS cells identifies a conserved response to LPS and novel alternative transcription

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    Author
    Alasoo, K; Martinez, FO; Hale, C; Gordon, S; Powrie, F; Dougan, G; Mukhopadhyay, S; Gaffney, DJ
    Date
    2015-07-30
    Source Title
    Scientific Reports
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Dougan, Gordon
    Affiliation
    Microbiology and Immunology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Alasoo, K., Martinez, F. O., Hale, C., Gordon, S., Powrie, F., Dougan, G., Mukhopadhyay, S. & Gaffney, D. J. (2015). Transcriptional profiling of macrophages derived from monocytes and iPS cells identifies a conserved response to LPS and novel alternative transcription. SCIENTIFIC REPORTS, 5 (1), https://doi.org/10.1038/srep12524.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259493
    DOI
    10.1038/srep12524
    Abstract
    Macrophages differentiated from human induced pluripotent stem cells (IPSDMs) are a potentially valuable new tool for linking genotype to phenotype in functional studies. However, at a genome-wide level these cells have remained largely uncharacterised. Here, we compared the transcriptomes of naïve and lipopolysaccharide (LPS) stimulated monocyte-derived macrophages (MDMs) and IPSDMs using RNA-Seq. The IPSDM and MDM transcriptomes were broadly similar and exhibited a highly conserved response to LPS. However, there were also significant differences in the expression of genes associated with antigen presentation and tissue remodelling. Furthermore, genes coding for multiple chemokines involved in neutrophil recruitment were more highly expressed in IPSDMs upon LPS stimulation. Additionally, analysing individual transcript expression identified hundreds of genes undergoing alternative promoter and 3' untranslated region usage following LPS treatment representing a previously under-appreciated level of regulation in the LPS response.

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