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Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3β activity
被引:372
作者:

Trivedi, Chinmay M.
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机构: Univ Penn, Sch Med, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA

Luo, Yang
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机构: Univ Penn, Sch Med, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA

Yin, Zhan
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机构: Univ Penn, Sch Med, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA

Zhang, Maozhen
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机构: Univ Penn, Sch Med, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA

Zhu, Wenting
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机构: Univ Penn, Sch Med, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA

Wang, Tao
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机构: Univ Penn, Sch Med, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA

Floss, Thomas
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机构: Univ Penn, Sch Med, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA

Goettlicher, Martin
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机构: Univ Penn, Sch Med, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA

Noppinger, Patricia Ruiz
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机构: Univ Penn, Sch Med, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA

Wurst, Wolfgang
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机构: Univ Penn, Sch Med, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA

Ferrari, Victor A.
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机构: Univ Penn, Sch Med, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA

Abrams, Charles S.
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机构: Univ Penn, Sch Med, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA

Gruber, Peter J.
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机构: Univ Penn, Sch Med, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA

Epstein, Jonathan A.
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机构: Univ Penn, Sch Med, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA
机构:
[1] Univ Penn, Sch Med, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA
[2] Univ Penn, Sch Med, Cardiovasc Inst, Philadelphia, PA 19104 USA
[3] Tech Univ Munich, D-85764 Neuherberg, Germany
[4] GSF Natl Res Ctr Environm & Hlth, Dept Toxicol, D-85764 Neuherberg, Germany
[5] Max Planck Inst Mol Genet, Dept Vertebrate Genom, D-10115 Berlin, Germany
[6] Univ Penn, Sch Med, Div Hematol Oncol, Philadelphia, PA 19104 USA
[7] Childrens Hosp Philadelphia, Cardiac Ctr, Philadelphia, PA 19104 USA
关键词:
D O I:
10.1038/nm1552
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
In the adult heart, a variety of stresses induce re-expression of a fetal gene program in association with myocyte hypertrophy and heart failure. Here we show that histone deacetylase-2 (Hdac2) regulates expression of many fetal cardiac isoforms. Hdac2 deficiency or chemical histone deacetylase ( HDAC) inhibition prevented the re-expression of fetal genes and attenuated cardiac hypertrophy in hearts exposed to hypertrophic stimuli. Resistance to hypertrophy was associated with increased expression of the gene encoding inositol polyphosphate-5-phosphatase f (Inpp5f) resulting in constitutive activation of glycogen synthase kinase 3b (Gsk3b) via inactivation of thymoma viral proto-oncogene (Akt) and 3-phosphoinositide- dependent protein kinase-1 (Pdk1). In contrast, Hdac2 transgenic mice had augmented hypertrophy associated with inactivated Gsk3b. Chemical inhibition of activated Gsk3b allowed Hdac2-deficient adults to become sensitive to hypertrophic stimulation. These results suggest that Hdac2 is an important molecular target of HDAC inhibitors in the heart and that Hdac2 and Gsk3b are components of a regulatory pathway providing an attractive therapeutic target for the treatment of cardiac hypertrophy and heart failure.
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页码:324 / 331
页数:8
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