Excessive O-GlcNAcylation of proteins suppresses spontaneous cardiogenesis in ES cells

Hoe Suk Kim, Sang Yoon Park, Yu Rim Choi, Jeong Gu Kang, Hyun Jung Joo, Woo Kyung Moon, Jin Won Cho

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Increased modification of proteins with O-linked N-acetylglucosamine (O-GlcNAc) has been implicated in the development of diabetic cardiomyopathy. We used the well-characterized ES cells (Nkx2.5GFP knock-in ES cells), to investigate the role of O-GlcNAcylation in cardiomyocyte development. O-GlcNAcylation decreased in differentiating ES cells, as did the expression of O-GlcNAc transferase. Increasing O-GlcNAcylation with glucosamine or by inhibiting N-acetylglucosaminidase (streptozotocin or PUGNAc) decreased the number of cardiomyocyte precursors and cardiac-specific gene expression. On the other hand, decreasing O-GlcNAcylation with an inhibitor of glutamine fructose-6-phosphate amidotransferase (6-diazo-5-oxo-norleucine) increased cardiomyocyte precursors. These results suggest that excessive O-GlcNAcylation impairs cardiac cell differentiation in ES cells.

Original languageEnglish
Pages (from-to)2474-2478
Number of pages5
JournalFEBS Letters
Issue number15
StatePublished - 6 Aug 2009


  • Cardiogenesis
  • Diabetes
  • Embryonic stem cell
  • Nkx2.5 transcription factor
  • O-GlcNAcylation
  • O-linked N-acetylglucosamine

Cite this

Kim, H. S., Park, S. Y., Choi, Y. R., Kang, J. G., Joo, H. J., Moon, W. K., & Cho, J. W. (2009). Excessive O-GlcNAcylation of proteins suppresses spontaneous cardiogenesis in ES cells. FEBS Letters, 583(15), 2474-2478. https://doi.org/10.1016/j.febslet.2009.06.052