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Muscle-derived follistatin-like 1 functions to reduce neointimal formation after vascular injury.
Miyabe, Megumi; Ohashi, Koji; Shibata, Rei; Uemura, Yusuke; Ogura, Yasuhiro; Yuasa, Daisuke; Kambara, Takahiro; Kataoka, Yoshiyuki; Yamamoto, Takashi; Matsuo, Kazuhiro; Joki, Yusuke; Enomoto, Takashi; Hayakawa, Satoko; Hiramatsu-Ito, Mizuho; Ito, Masanori; Van Den Hoff, Maurice J B; Walsh, Kenneth; Murohara, Toyoaki; Ouchi, Noriyuki.
Afiliación
  • Miyabe M; Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
  • Ohashi K; Department of Molecular Cardiology, Nagoya University Graduate School of Medicine, 65 Tsurumaicho, Showa-ku, Nagoya 466-8550, Japan nouchi@med.nagoya-u.ac.jp ohashik@med.nagoya-u.ac.jp.
  • Shibata R; Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
  • Uemura Y; Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
  • Ogura Y; Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
  • Yuasa D; Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
  • Kambara T; Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
  • Kataoka Y; Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
  • Yamamoto T; Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
  • Matsuo K; Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
  • Joki Y; Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
  • Enomoto T; Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
  • Hayakawa S; Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
  • Hiramatsu-Ito M; Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
  • Ito M; Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
  • Van Den Hoff MJ; Department of Anatomy, Embryology & Physiology, Heart Failure Research Center, Academic Medical Center, Amsterdam, Netherlands.
  • Walsh K; Department of Molecular Cardiology, Boston University School of Medicine, Boston, MA, USA.
  • Murohara T; Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
  • Ouchi N; Department of Molecular Cardiology, Nagoya University Graduate School of Medicine, 65 Tsurumaicho, Showa-ku, Nagoya 466-8550, Japan nouchi@med.nagoya-u.ac.jp ohashik@med.nagoya-u.ac.jp.
Cardiovasc Res ; 103(1): 111-20, 2014 Jul 01.
Article en En | MEDLINE | ID: mdl-24743592
AIMS: It is well-established that exercise diminishes cardiovascular risk, but whether humoral factors secreted by muscle confer these benefits has not been conclusively shown. We have shown that the secreted protein follistatin-like 1 (Fstl1) has beneficial actions on cardiac and endothelial function. However, the role of muscle-derived Fstl1 in proliferative vascular disease remains largely unknown. Here, we investigated whether muscle-derived Fstl1 modulates vascular remodelling in response to injury. METHODS AND RESULTS: The targeted ablation of Fstl1 in muscle led to an increase in neointimal formation following wire-induced arterial injury compared with control mice. Conversely, muscle-specific Fstl1 transgenic (TG) mice displayed a decrease in the neointimal thickening following arterial injury. Muscle-specific Fstl1 ablation and overexpression increased and decreased, respectively, the frequency of BrdU-positive proliferating cells in injured vessels. In cultured human aortic smooth muscle cells (HASMCs), treatment with human FSTL1 protein decreased proliferation and migration induced by stimulation with PDGF-BB. Treatment with FSTL1 enhanced AMPK phosphorylation, and inhibition of AMPK abrogated the inhibitory actions of FSTL1 on HASMC responses to PDGF-BB. The injured arteries of Fstl1-TG mice exhibited an increase in AMPK phosphorylation, and administration of AMPK inhibitor reversed the anti-proliferative actions of Fstl1 on the vessel wall. CONCLUSION: Our findings indicate that muscle-derived Fstl1 attenuates neointimal formation in response to arterial injury by suppressing SMC proliferation through an AMPK-dependent mechanism. Thus, the release of protein factors from muscle, such as Fstl1, may partly explain why the maintenance of muscle function can have a therapeutic effect on the cardiovascular system.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Proteínas Relacionadas con la Folistatina / Arteria Femoral / Neointima Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Cardiovasc Res Año: 2014 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Proteínas Relacionadas con la Folistatina / Arteria Femoral / Neointima Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Cardiovasc Res Año: 2014 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Reino Unido