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Excessive O-GlcNAcylation of proteins suppresses spontaneous cardiogenesis in ES cells |
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| Authors: | Hoe-Suk Kim Sang Yoon Park Yu Rim Choi Hyun Jung Joo Jin Won Cho |
| Institution: | a Medical Research Center, Seoul National University, 101 Daehangno, Jongno-gu, Seoul 110-744, Republic of Korea b Department of Diagnostic Radiology, Seoul National University Hospital, 101 Daehangno, Jongno-gu, Seoul 110-744, Republic of Korea c Department of Biology and WCU Program Department of Biomedical Science, Yonsei University, 134 Shinchon-dong, Seodaemun-gu, Seoul 120-749, Republic of Korea |
| 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. |
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