Scaffolds and chaperones in myofibril assembly: putting the striations in striated muscle

Crawford, Garland L.; Horowits, Robert

doi:10.1007/s12551-011-0043-x

Cited by 34 publications

(24 citation statements)

References 79 publications

(122 reference statements)

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“…The downregulation of N-RAP ( nebulin-related anchoring protein ) and zyxin , encoding proteins localized to the intercalated disc, has been demonstrated in cardiomyocyte-specific Prox1 mutant hearts (83, 114). Both of these genes were also identified as targets of Prox1 in global ChIP studies.…”

Section: Intercalated Discsmentioning

confidence: 99%

Transcriptional networks regulating the costamere, sarcomere, and other cytoskeletal structures in striated muscle

Estrella

Naya

2013

Cell. Mol. Life Sci.

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Structural abnormalities in striated muscle have been observed in numerous transcription factor gain- and loss-of-function phenotypes in animal and cell culture model systems, indicating that transcription is important in regulating the cytoarchitecture. While most characterized cytoarchitectural defects are largely indistinguishable by histological and ultrastructural criteria, analysis of dysregulated gene expression in each mutant phenotype has yielded valuable information regarding specific structural gene programs that may be uniquely controlled by each of these transcription factors. Linking the formation and maintenance of each subcellular structure or subset of proteins within a cytoskeletal compartment to an overlapping but distinct transcription factor cohort may enable striated muscle to control cytoarchitectural function in an efficient and specific manner. Here we summarize available evidence that connects transcription factors, those with established roles in striated muscle such as MEF2 and SRF as well as other non-muscle transcription factors, to the regulation of a defined cytoskeletal structure. The notion that genes encoding proteins localized to the same subcellular compartment are coordinately transcriptionally regulated may prompt rationally designed approaches that target specific transcription factor pathways to correct structural defects in muscle disease.

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Section: Intercalated Discsmentioning

confidence: 99%

Transcriptional networks regulating the costamere, sarcomere, and other cytoskeletal structures in striated muscle

Estrella

Naya

2013

Cell. Mol. Life Sci.

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“…Myofibers contain contractile fibril structures known as myofibrils that are composed of repeating units of sarcomeres. Sarcomeres primarily consist of thick filaments of myosin, thin filaments of actin, and elastic filaments of titin [12, 13]. Myofibrillogenesis, the development of the myofibril during myogenesis, plays a critical role in controlling the contractile strength of skeletal muscles [14, 15].…”

Section: Introductionmentioning

confidence: 99%

Controlled Heat Stress Promotes Myofibrillogenesis during Myogenesis

Guo¹,

Miller²,

An³

et al. 2016

PLoS ONE

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Hyperthermia therapy has recently emerged as a clinical modality used to finely tune heat stress inside the human body for various biomedical applications. Nevertheless, little is known regarding the optimal timing or temperature of heat stress that is needed to achieve favorable results following hyperthermia therapy for muscle regeneration purposes. The regeneration of skeletal muscle after injury is a highly complex and coordinated process that involves a multitude of cellular mechanisms. The main objective of this study was to characterize the effects of hyperthermal therapy on the overall behavior of myoblasts during myogenic differentiation. Various cellular processes, including myogenesis, myofibrillogenesis, hypertrophy/atrophy, and mitochondrial biogenesis, were studied using systematic cellular, morphological, and pathway-focused high-throughput gene expression profiling analyses. We found that C2C12 myoblasts exhibited distinctive time and temperature-dependence in biosynthesis and regulatory events during myogenic differentiation. Specifically, we for the first time observed that moderate hyperthermia at 39°C favored the growth of sarcomere in myofibrils at the late stage of myogenesis, showing universal up-regulation of characteristic myofibril proteins. Characteristic myofibrillogenesis genes, including heavy polypeptide 1 myosin, heavy polypeptide 2 myosin, alpha 1 actin, nebulin and titin, were all significantly upregulated (p<0.01) after C2C12 cells differentiated at 39°C over 5 days compared with the control cells cultured at 37°C. Furthermore, moderate hyperthermia enhanced myogenic differentiation, with nucleus densities per myotube showing 2.2-fold, 1.9-fold and 1.6-fold increases when C2C12 cells underwent myogenic differentiation at 39°C over 24 hours, 48 hours and 72 hours, respectively, as compared to the myotubes that were not exposed to heat stress. Yet, atrophy genes were sensitive even to moderate hyperthermia, indicating that strictly controlled heat stress is required to minimize the development of atrophy in myotubes. In addition, mitochondrial biogenesis was enhanced following thermal induction of myoblasts, suggesting a subsequent shift toward anabolic demand requirements for energy production. This study offers a new perspective to understand and utilize the time and temperature-sensitive effects of hyperthermal therapy on muscle regeneration.

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“…Within each sarcomere is a complex arrangement of proteins [2–4]. Each sarcomere is bounded by the Z-disk [5]. The Z-disk is crucial for maintaining sarcomeric structure and function.…”

Section: Introductionmentioning

confidence: 99%

Remodeling of the sarcomeric cytoskeleton in cardiac ventricular myocytes during heart failure and after cardiac resynchronization therapy

Lichter

Carruth

Mitchell

et al. 2014

Journal of Molecular and Cellular Cardiology

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Sarcomeres are the basic contractile units of cardiac myocytes. Recent studies demonstrated remodeling of sarcomeric proteins in several diseases, including genetic defects and heart failure. Here we investigated remodeling of sarcomeric α-actinin in two models of heart failure, synchronous (SHF) and dyssynchronous heart failure (DHF), as well as a model of cardiac resynchronization therapy (CRT). We applied three-dimensional confocal microscopy and quantitative methods of image analysis to study isolated cells from our animal models. 3D Fourier analysis revealed a decrease of the spatial regularity of the α-actinin distribution in both SHF and DHF versus control cells. The spatial regularity of α-actinin in DHF cells was reduced when compared with SHF cells. The spatial regularity of α-actinin was partially restored after CRT. We found longitudinal depositions of α-actinin in SHF, DHF and CRT cells. These depositions spanned adjacent Z-disks and exhibited a lower density of α-actinin than in the Z-disk. Differences in the occurrence of depositions between the SHF, CRT and DHF models versus control were significant. Also, CRT cells exhibited a higher occurrence of depositions versus SHF, but not DHF cells. Other sarcomeric proteins did not accumulate in the depositions to the same extent as α-actinin. We did not find differences in the expression of α-actinin protein and its encoding gene in our animal models. In summary, our studies indicate that HF is associated with two different types of remodeling of α-actinin and only one of those was reversed after CRT. We suggest that these results can guide us to an understanding of remodeling of structures and function associated with sarcomeres.

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Scaffolds and chaperones in myofibril assembly: putting the striations in striated muscle

Cited by 34 publications

References 79 publications

Transcriptional networks regulating the costamere, sarcomere, and other cytoskeletal structures in striated muscle

Transcriptional networks regulating the costamere, sarcomere, and other cytoskeletal structures in striated muscle

Controlled Heat Stress Promotes Myofibrillogenesis during Myogenesis

Remodeling of the sarcomeric cytoskeleton in cardiac ventricular myocytes during heart failure and after cardiac resynchronization therapy

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