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

Research output: Contribution to journal › Article › peer-review

28 Citations (Scopus)

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

Bibliographical note

Funding Information:
This work was supported by a Korea Research Foundation Grant funded by the Korean Government (MOEHRD; KRF-2006-311-C00399), grants from the Korea Science and Engineering Foundation (KOSEF) funded by the Ministry of Education, Science and Technology Grant (R0A-2007-000-20011-0), Korea Research Foundation Grant (KRF-2004-005-C00112) and WCU project (R31-2008-000-10086-0). S.Y.P. and J.G.K. are fellowship awardees of the Brain Korea 21 (BK21) program. This work was made possible through the use of research facilities in the Yonsei Center for Biotechnology. We thank Dr. T. Morisaki and K. Hidaka (National Cardiovascular Center Research Institute at Osaka, Japan) for providing mouse embryonic stem cell line.

All Science Journal Classification (ASJC) codes

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

UN SDGs

This output contributes to the following Sustainable Development Goal(s)

Access to Document

10.1016/j.febslet.2009.06.052

Fingerprint Dive into the research topics of 'Excessive O-GlcNAcylation of proteins suppresses spontaneous cardiogenesis in ES cells'. Together they form a unique fingerprint.

Cite this

@article{1154ad18e3914a69977d74e9c6762b5c,

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}",

note = "Funding Information: This work was supported by a Korea Research Foundation Grant funded by the Korean Government (MOEHRD; KRF-2006-311-C00399), grants from the Korea Science and Engineering Foundation (KOSEF) funded by the Ministry of Education, Science and Technology Grant (R0A-2007-000-20011-0), Korea Research Foundation Grant (KRF-2004-005-C00112) and WCU project (R31-2008-000-10086-0). S.Y.P. and J.G.K. are fellowship awardees of the Brain Korea 21 (BK21) program. This work was made possible through the use of research facilities in the Yonsei Center for Biotechnology. We thank Dr. T. Morisaki and K. Hidaka (National Cardiovascular Center Research Institute at Osaka, Japan) for providing mouse embryonic stem cell line. ",

year = "2009",

month = aug,

day = "6",

doi = "10.1016/j.febslet.2009.06.052",

language = "English",

volume = "583",

pages = "2474--2478",

journal = "FEBS Letters",

issn = "0014-5793",

publisher = "Elsevier",

number = "15",

}

TY - JOUR

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

N1 - Funding Information: This work was supported by a Korea Research Foundation Grant funded by the Korean Government (MOEHRD; KRF-2006-311-C00399), grants from the Korea Science and Engineering Foundation (KOSEF) funded by the Ministry of Education, Science and Technology Grant (R0A-2007-000-20011-0), Korea Research Foundation Grant (KRF-2004-005-C00112) and WCU project (R31-2008-000-10086-0). S.Y.P. and J.G.K. are fellowship awardees of the Brain Korea 21 (BK21) program. This work was made possible through the use of research facilities in the Yonsei Center for Biotechnology. We thank Dr. T. Morisaki and K. Hidaka (National Cardiovascular Center Research Institute at Osaka, Japan) for providing mouse embryonic stem cell line.

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.

UR - http://www.scopus.com/inward/record.url?scp=67849106344&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=67849106344&partnerID=8YFLogxK

U2 - 10.1016/j.febslet.2009.06.052

DO - 10.1016/j.febslet.2009.06.052

M3 - Article

C2 - 19591829

AN - SCOPUS:67849106344

VL - 583

SP - 2474

EP - 2478

JO - FEBS Letters

JF - FEBS Letters

SN - 0014-5793

IS - 15

ER -

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

Abstract

Bibliographical note

All Science Journal Classification (ASJC) codes

UN SDGs

Access to Document

Other files and links

Cite this