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

doi:10.1016/j.febslet.2009.06.052

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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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.

Original language	English
Pages (from-to)	2474-2478
Number of pages	5
Journal	FEBS Letters
Volume	583
Issue number	15
DOIs	https://doi.org/10.1016/j.febslet.2009.06.052
Publication status	Published - 2009 Aug 6

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All Science Journal Classification (ASJC) codes

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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

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title = "Excessive O-GlcNAcylation of proteins suppresses spontaneous cardiogenesis in ES cells",

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.",

author = "Kim, {Hoe Suk} and Park, {Sang Yoon} and Choi, {Yu Rim} and Kang, {Jeong Gu} and Joo, {Hyun Jung} and Moon, {Woo Kyung} and Cho, {Jin Won}",

year = "2009",

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T1 - Excessive O-GlcNAcylation of proteins suppresses spontaneous cardiogenesis in ES cells

AU - Kim, Hoe Suk

AU - Park, Sang Yoon

AU - Choi, Yu Rim

AU - Kang, Jeong Gu

AU - Joo, Hyun Jung

AU - Moon, Woo Kyung

AU - Cho, Jin Won

PY - 2009/8/6

Y1 - 2009/8/6

N2 - 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.

AB - 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.

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10.1016/j.febslet.2009.06.052