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FEBS Lett. 2009 Aug 6;583(15):2474-8. doi: 10.1016/j.febslet.2009.06.052. Epub 2009 Jul 8.

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

Author information

1
Medical Research Center, Seoul National University, Seoul, Republic of Korea. hoeskim@hotmail.com

Abstract

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.

PMID:
19591829
DOI:
10.1016/j.febslet.2009.06.052
[Indexed for MEDLINE]
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