Myofibrillogenesis regulator 1 induces hypertrophy by promoting sarcomere organization in neonatal rat cardiomyocytes
| Autor: | Xiaoreng Wang, Kang Luan, Song Wang, Xiuhua Liu |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
Sarcomeres
myofibrillogenesis regulator Physiology SUMO-1 Protein Muscle Proteins Chromosomal translocation cardiomyocyte Biology Muscle Development Transfection Muscle hypertrophy Rats Sprague-Dawley Internal Medicine Animals Connectin Myocytes Cardiac Sarcomere organization Cells Cultured Neonatal rat Hypertrophy Myofibrillogenesis regulator 1 Molecular biology sarcomere organization Cell biology Rats Animals Newborn Cytoplasm embryonic structures Models Animal Original Article Cardiology and Cardiovascular Medicine Nuclear localization sequence |
| Zdroj: | Hypertension Research |
| ISSN: | 1348-4214 |
| Popis: | Human myofibrillogenesis regulator 1, a novel 17-kDa protein, is closely involved in cardiac hypertrophy. We studied the molecular mechanism that links MR-1 to hypertrophic response. Hypertrophic hallmarks such as cell size and [(3)H]-leucine incorporation were significantly increased when MR-1 was transfected into cardiomyocytes for 48 h. However, sarcomere organization was promoted when MR-1 was transfected for 8 h. The finding that cardiac hypertrophy was induced long after increase of sarcomere organization indicates that the promoted sarcomere organization may be one of the crucial factors causing hypertrophy. Furthermore, when MR-1 was transfected into cardiomyocytes, the nuclear localization of myomesin-1 was shifted to the cytoplasm. Transfection with small ubiquitin-like modifier-1 (SUMO-1) mimicked the effect of MR-1 inducing translocation of myomesin-1. However, transfection with SUMO-1 in MR-1-silenced cardiomyocytes failed to induce translocation and sarcomere organization, even though SUMO-1 expression was at the same level. Overexpression of MR-1 may induce cardiomyocyte hypertrophy via myomesin-1-mediated sarcomere organization. |
| Databáze: | OpenAIRE |
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