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

Wang, Xiao-Reng; Li, Xiuhua; Wang, Song; Luan, Kang

doi:10.1038/hr.2011.228

Cited by 18 publications

(41 citation statements)

References 25 publications

(38 reference statements)

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“…It is closely associated with F-actin polymerization in neonatal rat cardiomyocytes [8,9] and the human liver cancer cell line HepG2 [10]. In the present study, MR-1 expression was reduced in I/R-treated rat kidney and H/R-treated HK-2 cells.…”

Section: Discussionsupporting

confidence: 49%

“…Samples containing 50 μg of protein were prepared and separated on 8-12% acrylamide gels and transferred to nitrocellulose membranes and blocked with 5% BSA in Tris-buffered saline Tween (20 mmol/l Tris-HCl, pH 7.5, 137 mmol/l NaCl, and 0.1% Tween 20). Membranes were incubated with antibodies against MR-1 (1:100) [9], MLC-2 (1:1,000; Abcam), pan-actin (1:500; Cell Signaling Technology, USA), and GAPDH (1:500; Abcam) overnight at 4°C. …”

Section: Methodsmentioning

confidence: 99%

“…Cells were incubated with primary antibodies against MR-1 (polyclonal rabbit, 1:50)[9], MLC-2 (polyclonal goat, 1:100; Santa Cruz Biotechnology, Santa Cruz, Calif., USA), and MLC kinase (MLCK) (monoclonal rabbit, 1:100; Abcam, UK) overnight at 4°C. The cells were then incubated with fluorescently labeled secondary antibodies: Texas red-conjugated donkey anti-rabbit (1:200; Santa Cruz Biotechnology) and FITC-conjugated donkey anti-goat (1:200; Santa Cruz Biotechnology).…”

Section: Methodsmentioning

confidence: 99%

“…Our previous work showed that MLC-2 interacted with a novel protein, myofibrillogenesis regulator (MR)-1, which is expressed in the kidney, striated muscle, liver, and brain of mammals [8]. We found that MR-1 promoted actin filament arrangement in myofibrils in neonatal cardiomyocytes [9]. MR-1 markedly promoted proliferation, migration, and fibrous actin (F-actin) polymerization through MLC-2 in human HepG2 cells [10].…”

Section: Introductionmentioning

confidence: 99%

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Kidney Protection against Ischemia/Reperfusion Injury by Myofibrillogenesis Regulator-1

Wang

Tao²,

Ding³

et al. 2014

Am J Nephrol

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Background/Aims: Ischemia/reperfusion (I/R) injury is characterized by cytoskeletal reorganization and loss of polarity in proximal tubule epithelial cells. Previously, we showed that myofibrillogenesis regulator (MR)-1 promoted actin organization in cardiomyocytes. MR-1 is also expressed in the kidney. Methods: In this study, we investigated MR-1 expression in acute renal failure induced by I/R in Sprague-Dawley rats. We determined the MR-1 expression and the ratio of fibrous actin (F-actin) to globular actin (G-actin). HK-2 cells were treated with or without hypoxia/reoxygenation (H/R), and MR-1 levels were increased by adenoviral overexpression or silenced by RNA interference. Results: I/R and H/R resulted in cellular injury and decreases of MR-1, the F-/G-actin ratio, and myosin light chain (MLC)-2. MR-1 overexpression attenuated H/R-induced cell injury and loss of surface membrane polarity of actin. MR-1 overexpression also increased the expression and phosphorylation of MLC-2 and MLC kinase, which were decreased in MR-1-silenced and H/R-treated cells. Conclusion: Together, these data show that MR-1 promoted actin polarity on the membrane surface and protected HK-2 cells from H/R injury. The mechanism might involve the rapid organization of F-actin through the upregulation and phosphorylation of MLC-2.

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Section: Discussionsupporting

confidence: 49%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Kidney Protection against Ischemia/Reperfusion Injury by Myofibrillogenesis Regulator-1

Wang

Tao²,

Ding³

et al. 2014

Am J Nephrol

Self Cite

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“…To quantify the size of imaged cardiomyocytes, the space between each striation (illustrated by the distance between myomesin bands stained green and actin bands stained red) was accepted as 2um as previously described (Wang X et al, 2012;Klabunde R, 2007 Previous studies have shown that GATA4 activation by phosphorylation of serine 105 occurs during hypertrophic-induced pathways (van Berlo et al, 2001). In order to study our first aim in understanding the roles of GATA4 and CARP within such hypertrophic pathways, NRVMs were stimulated with PE or 7% FBS hypertrophic-inducing agents.…”

Section: Aim Two Immunofluorescencementioning

confidence: 99%

CARP Plays a Key Role in Cellular Growth Under Hypertrophic Stimuli in Neonatal Rat Ventricular Myocytes

Shrout

2013

VURJ

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Cardiac hypertrophy is a growth process characterized by an increase in individual myocyte size and overall cardiac muscle mass. Although such growth can occur through physiological means such as exercise, this study examined molecular components of the pathological process that occurs in response to long-term stress, injury, or disease states. Such hypertrophic stimuli induce unique cardiac muscle growth, increasing the risk of ischemia and congestive heart failure. During the pathological process, the fundamental unit of cardiac muscle-the sarcomere-is disrupted, both as a consequence of changes in gene expression and local sarcomeric proteins. Cardiac-restricted ankyrin repeat protein (CARP) is a crucial protein that functions both in the cardiac sarcomere and at the nuclear transcriptional level. We postulated that due to this dual nature, CARP plays a key role in maintaining the cardiac sarcomere and inducing hypertrophic growth pathways. GATA4 is a transcription factor with known importance during cardiac hypertrophy. Our studies uniquely suggest that CARP and GATA4 interact, and affirm that GATA4 is activated by hypertrophic stimuli. In order to partly delineate the complex process of cardiac hypertrophy, we applied a novel approach by testing cardiomyocytes for changes in CARP levels and GATA4 activation after hypertrophic stimuli over time. Neonatal Rat Ventricular Myocytes (NRVMs) were used in this study, and induced by the stimuli agents of phenylephrine (PE) and fetal bovine serum (FBS). Aggregate results of changes in GATA4 activation over time after both stimuli did not generate a consistent trend over time and did not gain statistically significance. CARP levels over time after such stimuli, however, were documented for the first known time, and generated a relative trend of increasing then decreasing levels over time after both stimuli with relatively more significance after PE stimuli. The functional role of CARP during hypertrophic growth was clearly and significantly demonstrated in this study through immunofluorescence. Results show that hypertrophic cardiomyocyte growth was significantly blunted when NRVMs were co-treated with CARP small-interfering RNA (siRNA), which disrupts CARP function. These data suggest that CARP plays a crucial role in the hypertrophic response in cardiomyocytes, and catalyzes further study.Summer 2013 | Volume 9 |

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Thick Filament Protein Network, Functions, and Disease Association

Wang

Geist

Grogan

et al. 2018

Comprehensive Physiology

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Sarcomeres consist of highly ordered arrays of thick myosin and thin actin filaments along with accessory proteins. Thick filaments occupy the center of sarcomeres where they partially overlap with thin filaments. The sliding of thick filaments past thin filaments is a highly regulated process that occurs in an ATP-dependent manner driving muscle contraction. In addition to myosin that makes up the backbone of the thick filament, four other proteins which are intimately bound to the thick filament, myosin binding protein-C, titin, myomesin, and obscurin play important structural and regulatory roles. Consistent with this, mutations in the respective genes have been associated with idiopathic and congenital forms of skeletal and cardiac myopathies. In this review, we aim to summarize our current knowledge on the molecular structure, subcellular localization, interacting partners, function, modulation via posttranslational modifications, and disease involvement of these five major proteins that comprise the thick filament of striated muscle cells. © 2018 American Physiological Society. Compr Physiol 8:631-709, 2018.

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

Cited by 18 publications

References 25 publications

Kidney Protection against Ischemia/Reperfusion Injury by Myofibrillogenesis Regulator-1

Kidney Protection against Ischemia/Reperfusion Injury by Myofibrillogenesis Regulator-1

CARP Plays a Key Role in Cellular Growth Under Hypertrophic Stimuli in Neonatal Rat Ventricular Myocytes

Thick Filament Protein Network, Functions, and Disease Association

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