Stem Cells
Stem Cells
5 years ago

Small Molecule Antagonist Of Cell Surface Glycosaminoglycans Restricts Mouse Embryonic Stem Cells In A Pluripotent State

Small Molecule Antagonist Of Cell Surface Glycosaminoglycans Restricts Mouse Embryonic Stem Cells In A Pluripotent State
Mia L. Huang, Kamil Godula, Christopher J. Fisher, Raymond A. A. Smith, Mitchell Christy, Austen L. Michalak
Recently, the field of stem2714 cell-based regeneration has turned its attention towards chemical approaches for controlling the pluripotency and differentiation of embryonic stem2714 cells using drug-like small molecule modulators. Growth factor receptors or their associated downstream kinases that regulate intracellular signaling pathways during differentiation are typically the targets for these molecules. The glycocalyx, which plays an essential role in actuating responses to growth factors at the cellular boundary, offers an underexplored opportunity for intervention using small molecules to influence differentiation. Here, we show that surfen, an antagonist of cell-surface glycosaminoglycans required for growth factor association with cognate receptors, acts as a potent and general inhibitor of differentiation and promoter of pluripotency in mouse embryonic stem2714 cells. This finding shows that drugging the stem2714 cell Glycome with small molecules to silence differentiation cues can provide a powerful new alternative to existing techniques for controlling stem2714 cell fate. This article is protected by copyright. All rights reserved. The stem cell glycocalyx presents an attractive opportunity for pharmacological targeting with small molecules to control pluripotency and cellular differentiation. Here, we demonstrate that the small molecule, surfen, maintains mouse embryonic stem cell pluripotency by antagonizing heparan sulfate glycosaminoglycans in the stem cell glycocalyx. By blocking binding sites for FGF2, it silences MAPK signaling and gene expression. Image magnification: 20X.

Publisher URL: http://onlinelibrary.wiley.com/resolve/doi

DOI: 10.1002/stem.2714

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