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dc.contributor.authorHng, CH
dc.contributor.authorCamp, E
dc.contributor.authorAnderson, P
dc.contributor.authorBreen, J
dc.contributor.authorZannettino, A
dc.contributor.authorGronthos, S
dc.date.accessioned2020-12-09T22:41:37Z
dc.date.available2020-12-09T22:41:37Z
dc.date.issued2020-07-09
dc.identifierpii: 10.1038/s41598-020-68261-2
dc.identifier.citationHng, 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.
dc.identifier.issn2045-2322
dc.identifier.urihttp://hdl.handle.net/11343/253043
dc.description.abstractPrevious 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.
dc.languageeng
dc.publisherSpringer Science and Business Media LLC
dc.titleHOPX regulates bone marrow-derived mesenchymal stromal cell fate determination via suppression of adipogenic gene pathways.
dc.typeJournal Article
dc.identifier.doi10.1038/s41598-020-68261-2
melbourne.affiliation.departmentPaediatrics (RCH)
melbourne.source.titleScientific Reports
melbourne.source.volume10
melbourne.source.issue1
melbourne.source.pages11345-
dc.rights.licenseCC BY
melbourne.elementsid1480988
melbourne.openaccess.pmchttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC7347885
melbourne.contributor.authorAnderson, Peter
dc.identifier.eissn2045-2322
melbourne.accessrightsOpen Access


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