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Involvement of peptidyl-prolyl isomerase Pin1 in the inhibitory effect of fluvastatin on endothelin-1-induced cardiomyocyte hypertrophy.

Authors
  • Sakai, Satoshi1
  • Shimojo, Nobutake2
  • Kimura, Taizo3
  • Tajiri, Kazuko3
  • Maruyama, Hidekazu3
  • Homma, Satoshi3
  • Kuga, Keisuke3
  • Mizutani, Taro2
  • Aonuma, Kazutaka3
  • Miyauchi, Takashi4
  • 1 Division of Cardiovascular Medicine, Department of Clinical Medicine, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan. Electronic address: [email protected] , (Japan)
  • 2 Division of Emergency and Critical Care Medicine, Department of Clinical Medicine, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan. , (Japan)
  • 3 Division of Cardiovascular Medicine, Department of Clinical Medicine, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan. , (Japan)
  • 4 Division of Cardiovascular Medicine, Department of Clinical Medicine, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan; Division of Life Science Center for Tsukuba Advanced Research Alliance (TARA), University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan. , (Japan)
Type
Published Article
Journal
Life sciences
Publication Date
May 02, 2014
Volume
102
Issue
2
Pages
98–104
Identifiers
DOI: 10.1016/j.lfs.2014.03.018
PMID: 24657892
Source
Medline
Keywords
License
Unknown

Abstract

This is the first report that ET-1-induced cardiomyocyte hypertrophy is mediated through the Pin1 activation and that the inhibitory effect of fluvastatin on cardiomyocyte hypertrophy would partly be attributed to the suppression of the Pin1 function. This study firstly suggests that Pin1 determines the size of hypertrophied cardiomyocyte by regulating the activity of phosphorylated molecules and that statins exert their pleiotropic effects partly via Pin1 inactivation.

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