NDLI: Rheb (Ras homologue enriched in brain)-dependent mammalian target of rapamycin complex 1 (mTORC1) activation becomes indispensable for cardiac hypertrophic growth after early postnatal period.

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Rheb (Ras homologue enriched in brain)-dependent mammalian target of rapamycin complex 1 (mTORC1) activation becomes indispensable for cardiac hypertrophic growth after early postnatal period.

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Rheb (Ras homologue enriched in brain)-dependent mammalian target of rapamycin complex 1 (mTORC1) activation becomes indispensable for cardiac hypertrophic growth after early postnatal period.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Shah, Ajay M. Tamai, Takahito Horie, Kyoji Oka, Takafumi Takeda, Junji Nakayama, Hiroyuki Uno, Yoshihiro Komuro, Issei Yamaguchi, Osamu Oyabu, Jota Hikoso, Shungo Taneike, Manabu Takeda, Toshihiro Sonenberg, Nahum Murakawa, Tomokazu Otsu, Kinya Nishida, Kazuhiko
Description	Author Affiliation: Tamai T ( Department of Cardiovascular Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan.)
Abstract	Cardiomyocytes proliferate during fetal life but lose their ability to proliferate soon after birth and further increases in cardiac mass are achieved through an increase in cell size or hypertrophy. Mammalian target of rapamycin complex 1 (mTORC1) is critical for cell growth and proliferation. Rheb (Ras homologue enriched in brain) is one of the most important upstream regulators of mTORC1. Here, we attempted to clarify the role of Rheb in the heart using cardiac-specific Rheb-deficient mice (Rheb(-/-)). Rheb(-/-) mice died from postnatal day 8 to 10. The heart-to-body weight ratio, an index of cardiomyocyte hypertrophy, in Rheb(-/-) was lower than that in the control (Rheb(+/+)) at postnatal day 8. The cell surface area of cardiomyocytes isolated from the mouse hearts increased from postnatal days 5 to 8 in Rheb(+/+) mice but not in Rheb(-/-) mice. Ultrastructural analysis indicated that sarcomere maturation was impaired in Rheb(-/-) hearts during the neonatal period. Rheb(-/-) hearts exhibited no difference in the phosphorylation level of S6 or 4E-BP1, downstream of mTORC1 at postnatal day 3 but showed attenuation at postnatal day 5 or 8 compared with the control. Polysome analysis revealed that the mRNA translation activity decreased in Rheb(-/-) hearts at postnatal day 8. Furthermore, ablation of eukaryotic initiation factor 4E-binding protein 1 in Rheb(-/-) mice improved mRNA translation, cardiac hypertrophic growth, sarcomere maturation, and survival. Thus, Rheb-dependent mTORC1 activation becomes essential for cardiomyocyte hypertrophic growth after early postnatal period.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	14
Volume Number	288
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2013-04-05
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Gene Expression Regulation, Developmental Heart Growth & Development Monomeric GTP-Binding Proteins Metabolism Neuropeptides TOR Serine-Threonine Kinases Chemistry Animals Animals, Newborn Autophagy Blotting, Southern Carrier Proteins Cell Proliferation Chromosomes, Artificial, Bacterial Echocardiography Physiology Hypertrophy Mice Mice, Inbred C57BL Mice, Transgenic Models, Biological Models, Genetic Muscle Cells Cytology Myocardium Phosphoproteins Polyribosomes Protein Biosynthesis Signal Transduction Time Factors Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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