Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3β activity (original) (raw)

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Acknowledgements

We thank J. Tobias for his help with microarray data analysis; A. Granger and M. Levin for assistance with cardiac myocyte isolation; K.J. Duffy for his help with analysis of echocardiography data; R. Zhou for assistance with magnetic resonance imaging; and T. Force (Thomas Jefferson University) for dn_Akt_ and ca_Akt_ adenovirus and constructs, and for advice with the manuscript. This work was supported by the US National Institutes of Health (RO1 HL071546 to J.A.E.). J.A.E. holds the W.W. Smith Endowed Chair for Cardiovascular Research at the University of Pennsylvania. C.M.T. is supported by an American Heart Association postdoctoral fellowship.

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Author notes

1. Yang Luo, Zhan Yin & Maozhen Zhang
   Present address: Present addresses: Novartis Institutes of Biomedical Research, 100 Technology Square, Cambridge, Massachusetts 02139, USA (Y.L.), Institute of Hydrobiology, Chinese Academy of Sciences, 7 Donghu South Road, Wuhan 430072, China (Z.Y.) and Department of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kong Jiang Road, Shanghai 200092, China (M.Z.).,
2. Chinmay M Trivedi, Yang Luo and Zhan Yin: These authors contributed equally to the work.

Authors and Affiliations

1. Department of Cell and Developmental Biology, 1156 Basic Research Building II, University of Pennsylvania School of Medicine, 421 Curie Boulevard, Philadelphia, 19104, Pennsylvania, USA
   Chinmay M Trivedi, Wenting Zhu & Jonathan A Epstein
2. Cardiovascular Institute, 956 Basic Research Building II, University of Pennsylvania School of Medicine, 421 Curie Boulevard, Philadelphia, 19104, Pennsylvania, USA
   Chinmay M Trivedi, Yang Luo, Zhan Yin, Maozhen Zhang, Tao Wang, Victor A Ferrari, Peter J Gruber & Jonathan A Epstein
3. Institute of Developmental Genetics, GSF National Research Center for Environment and Health, Ingolstaedter Landstrasse 1, Neuherberg, 85764, Germany
   Thomas Floss & Wolfgang Wurst
4. Technical University Munich and Toxicology Department of the GSF National Research Center for Environment and Health, Ingolstaedter Landstrasse 1, Neuherberg, 85764, Germany
   Martin Goettlicher
5. Department of Vertebrate Genomics, Max-Planck Institute for Molecular Genetics, Hessische Str. 3-4, Berlin, 10115, Germany
   Patricia Ruiz Noppinger
6. Hematology-Oncology Division, 912 Basic Research Building II, University of Pennsylvania School of Medicine, 421 Curie Boulevard, Philadelphia, 19104, Pennsylvania, USA
   Charles S Abrams
7. The Cardiac Center, 905 Basic Research Building II, Children's Hospital of Philadelphia, 421 Curie Boulevard, Philadelphia, 19104, Pennsylvania, USA
   Peter J Gruber

Authors

1. Chinmay M Trivedi
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2. Yang Luo
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3. Zhan Yin
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4. Maozhen Zhang
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5. Wenting Zhu
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6. Tao Wang
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7. Thomas Floss
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8. Martin Goettlicher
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9. Patricia Ruiz Noppinger
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10. Wolfgang Wurst
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11. Victor A Ferrari
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12. Charles S Abrams
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13. Peter J Gruber
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14. Jonathan A Epstein
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Contributions

C.M.T. contributed significantly to the writing of the manuscript. M.Z. performed histological sectioning of embryo and heart tissue. W.Z. assisted with siRNA experiments. T.W. performed TAC surgery. T.F., M.G., P.R.N. and W.W. created the Hdac2 gene-trap ES line. V.A.F. carried out echocardiography and MRI studies. C.S.A. helped with PI3K activity experiments and provided advice related to PI3K signaling. P.J.G. was instrumental during early stages of the project and initiated Hdac2 expression studies. J.A.E. conceived, designed and directed the study, supervised C.M.T., Y.L., Z.Y., M.Z., T.W. and W.Z., and wrote the manuscript.

Corresponding author

Correspondence toJonathan A Epstein.

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Competing interests

Y.L. declares that he is presently employed by Novartis Pharmaceuticals, though he did not work for Novartis at the time that the work was performed in the Epstein lab. V.F. declares that he receives grant support from GlaxoSmithKline, Inc. Other authors declare no competing financial interests.

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Trivedi, C., Luo, Y., Yin, Z. et al. Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3β activity.Nat Med 13, 324–331 (2007). https://doi.org/10.1038/nm1552

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• Received: 10 October 2006
• Accepted: 17 January 2007
• Published: 18 February 2007
• Issue Date: March 2007
• DOI: https://doi.org/10.1038/nm1552