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    HOPX regulates bone marrow-derived mesenchymal stromal cell fate determination via suppression of adipogenic gene pathways.

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    Author
    Hng, CH; Camp, E; Anderson, P; Breen, J; Zannettino, A; Gronthos, S
    Date
    2020-07-09
    Source Title
    Scientific Reports
    Publisher
    Springer Science and Business Media LLC
    University of Melbourne Author/s
    Anderson, Peter
    Affiliation
    Paediatrics (RCH)
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Hng, C. H., Camp, E., Anderson, P., Breen, J., Zannettino, A. & Gronthos, S. (2020). HOPX regulates bone marrow-derived mesenchymal stromal cell fate determination via suppression of adipogenic gene pathways.. Sci Rep, 10 (1), pp.11345-. https://doi.org/10.1038/s41598-020-68261-2.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/253043
    DOI
    10.1038/s41598-020-68261-2
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7347885
    Abstract
    Previous studies of global binding patterns identified the epigenetic factor, EZH2, as a regulator of the homeodomain-only protein homeobox (HOPX) gene expression during bone marrow stromal cell (BMSC) differentiation, suggesting a potential role for HOPX in regulating BMSC lineage specification. In the present study, we confirmed that EZH2 direct binds to the HOPX promoter region, during normal growth and osteogenic differentiation but not under adipogenic inductive conditions. HOPX gene knockdown and overexpression studies demonstrated that HOPX is a promoter of BMSC proliferation and an inhibitor of adipogenesis. However, functional studies failed to observe any affect by HOPX on BMSC osteogenic differentiation. RNA-seq analysis of HOPX overexpressing BMSC during adipogenesis, found HOPX function to be acting through suppression of adipogenic pathways associated genes such as ADIPOQ, FABP4, PLIN1 and PLIN4. These findings suggest that HOPX gene target pathways are critical factors in the regulation of fat metabolism.

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