Limits...
Myofibrillogenesis regulator 1 induces hypertrophy by promoting sarcomere organization in neonatal rat cardiomyocytes.

Wang X, Liu X, Wang S, Luan K - Hypertens. Res. (2012)

Bottom Line: Hypertrophic hallmarks such as cell size and [(3)H]-leucine incorporation were significantly increased when MR-1 was transfected into cardiomyocytes for 48 h.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathophysiology, PLA General Hospital, Beijing, China.

ABSTRACT
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.

Show MeSH

Related in: MedlinePlus

Subcellular localization and organization of MR-1 in cardiac myofibrils indicated by antibody of MR-1, α-actinin and MLC-2. (a) Double immunofluorescent staining of MR-1 (red) with α-actinin (green) showing regular striated pattern of MR-1 (red) in the areas where α-actinin (green) is negatively stained. (b) MR-1 is co-localized with MLC-2 and merged in A-band. (c) Staining of MR-1 in neonatal rat cardiomyocytes. Control: the punctated, thin, rudimentary filaments of MR-1 are shown in the normal cultured cardiomyocytes. MR-1: striated pattern of MR-1 staining shown in a cardiomyocyte transfected with MR-1. Vector: both nonstriated and striated MR-1 filaments shown in one cardiomyocyte transfected with vector plasmid.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3368235&req=5

fig2: Subcellular localization and organization of MR-1 in cardiac myofibrils indicated by antibody of MR-1, α-actinin and MLC-2. (a) Double immunofluorescent staining of MR-1 (red) with α-actinin (green) showing regular striated pattern of MR-1 (red) in the areas where α-actinin (green) is negatively stained. (b) MR-1 is co-localized with MLC-2 and merged in A-band. (c) Staining of MR-1 in neonatal rat cardiomyocytes. Control: the punctated, thin, rudimentary filaments of MR-1 are shown in the normal cultured cardiomyocytes. MR-1: striated pattern of MR-1 staining shown in a cardiomyocyte transfected with MR-1. Vector: both nonstriated and striated MR-1 filaments shown in one cardiomyocyte transfected with vector plasmid.

Mentions: To directly assess whether MR-1 is involved in sarcomere organization, MR-1 and sarcomere A-band marker MRLC and Z-line marker α-actinin were double stained, respectively, in the 48-h-normal-cultured cardiomyocytes. The staining of MR-1 mainly existed in the area with negative staining for α-actinin (Figure 2a) but positive staining for MRLC (Figure 2b). MR-1 was co-located with MRLC. A dark zone was observed in the middle of the brightly stained MR-1 band (Figure 2b, arrow), clearly indicating the H-zone of a sarcomere. Thus, MR-1 could be incorporated into sarcomere A-bands between Z-lines.


Myofibrillogenesis regulator 1 induces hypertrophy by promoting sarcomere organization in neonatal rat cardiomyocytes.

Wang X, Liu X, Wang S, Luan K - Hypertens. Res. (2012)

Subcellular localization and organization of MR-1 in cardiac myofibrils indicated by antibody of MR-1, α-actinin and MLC-2. (a) Double immunofluorescent staining of MR-1 (red) with α-actinin (green) showing regular striated pattern of MR-1 (red) in the areas where α-actinin (green) is negatively stained. (b) MR-1 is co-localized with MLC-2 and merged in A-band. (c) Staining of MR-1 in neonatal rat cardiomyocytes. Control: the punctated, thin, rudimentary filaments of MR-1 are shown in the normal cultured cardiomyocytes. MR-1: striated pattern of MR-1 staining shown in a cardiomyocyte transfected with MR-1. Vector: both nonstriated and striated MR-1 filaments shown in one cardiomyocyte transfected with vector plasmid.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3368235&req=5

fig2: Subcellular localization and organization of MR-1 in cardiac myofibrils indicated by antibody of MR-1, α-actinin and MLC-2. (a) Double immunofluorescent staining of MR-1 (red) with α-actinin (green) showing regular striated pattern of MR-1 (red) in the areas where α-actinin (green) is negatively stained. (b) MR-1 is co-localized with MLC-2 and merged in A-band. (c) Staining of MR-1 in neonatal rat cardiomyocytes. Control: the punctated, thin, rudimentary filaments of MR-1 are shown in the normal cultured cardiomyocytes. MR-1: striated pattern of MR-1 staining shown in a cardiomyocyte transfected with MR-1. Vector: both nonstriated and striated MR-1 filaments shown in one cardiomyocyte transfected with vector plasmid.
Mentions: To directly assess whether MR-1 is involved in sarcomere organization, MR-1 and sarcomere A-band marker MRLC and Z-line marker α-actinin were double stained, respectively, in the 48-h-normal-cultured cardiomyocytes. The staining of MR-1 mainly existed in the area with negative staining for α-actinin (Figure 2a) but positive staining for MRLC (Figure 2b). MR-1 was co-located with MRLC. A dark zone was observed in the middle of the brightly stained MR-1 band (Figure 2b, arrow), clearly indicating the H-zone of a sarcomere. Thus, MR-1 could be incorporated into sarcomere A-bands between Z-lines.

Bottom Line: Hypertrophic hallmarks such as cell size and [(3)H]-leucine incorporation were significantly increased when MR-1 was transfected into cardiomyocytes for 48 h.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathophysiology, PLA General Hospital, Beijing, China.

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus