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dc.contributor.authorVethe, Heidrunen_US
dc.contributor.authorGhila, Luizaen_US
dc.contributor.authorBerle, Magnusen_US
dc.contributor.authorHoareau, Laurenceen_US
dc.contributor.authorHaaland, Øystein Ariansenen_US
dc.contributor.authorScholz, Hanneen_US
dc.contributor.authorPaulo, Joao A.en_US
dc.contributor.authorChera, Simonaen_US
dc.contributor.authorRæder, Helgeen_US
dc.PublishedVethe H, Ghila L, Berle MF, Hoareau ML, Haaland ØA, Scholz HS, Paulo JA, Chera S, Ræder H. Modulating Wnt signaling in human induced pluripotent stem cell-derived S7 cells. Frontiers in Endocrinology. 2019;10:293eng
dc.description.abstractCurrent published protocols for targeted differentiation of human stem cells toward pancreatic β-cells fail to deliver sufficiently mature cells with functional properties comparable to human islet β-cells. We aimed to assess whether Wnt-modulation could promote the final protocol stages of β-cell maturation, building our hypothesis on our previous findings of Wnt activation in immature hiPSC-derived stage 7 (S7) cells compared to adult human islets and with recent data reporting a link between Wnt/PCP and in vitro β-cell maturation. In this study, we stimulated canonical and non-canonical Wnt signaling in hiPSC-derived S7 cells using syntetic proteins including WNT3A, WNT4, WNT5A and WNT5B, and we inhibited endogenous Wnt signaling with the Tankyrase inhibitor G007-LK (TKi). Whereas neither canonical nor non-canonical Wnt stimulation alone was able to mature hiPSC-derived S7 cells, WNT-inhibition with TKi increased the fraction of monohormonal cells and global proteomics of TKi-treated S7 cells showed a proteomic signature more similar to adult human islets, suggesting that inhibition of endogenous Wnt contributes toward final β-cell maturation.en_US
dc.rightsAttribution CC BYeng
dc.titleModulating Wnt signaling in human induced pluripotent stem cell-derived S7 cellsen_US
dc.typePeer reviewed
dc.typeJournal article
dc.rights.holderCopyright 2019 The Author(s)
dc.source.journalFrontiers in Endocrinology
dc.relation.projectNorges forskningsråd: 262613

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