Extracellular-matrix synthesis by skeletal muscle in culture. Major secreted collagenous proteins of clonal myoblasts

Beach, Robert L.; Rao, Jasti S.; Festoff, Barry W.

doi:10.1042/bj2250619

Cited by 16 publications

(8 citation statements)

References 51 publications

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“…ECM is important in muscle maintenance and regulation of muscle development and growth and is essential for myotube formation [ 45 , 46 ]. A majority of the components of the ECM are produced by fibroblasts [ 47 ], but both muscle precursor cells (satellite cells) and multinucleated myofibers have been shown to contribute to the production of ECM [ 48 – 50 ]. Perhaps the up-regulation of genes involved in the ECM in combination with down-regulation of myogenesis and muscle function is a compensating mechanism, although this needs to be further investigated.…”

Section: Discussionmentioning

confidence: 99%

Type 2 diabetes and obesity induce similar transcriptional reprogramming in human myocytes

et al. 2017

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BackgroundSkeletal muscle is one of the primary tissues involved in the development of type 2 diabetes (T2D). The close association between obesity and T2D makes it difficult to isolate specific effects attributed to the disease alone. Therefore, here we set out to identify and characterize intrinsic properties of myocytes, associated independently with T2D or obesity.MethodsWe generated and analyzed RNA-seq data from primary differentiated myotubes from 24 human subjects, using a factorial design (healthy/T2D and non-obese/obese), to determine the influence of each specific factor on genome-wide transcription. This setup enabled us to identify intrinsic properties, originating from muscle precursor cells and retained in the corresponding myocytes. Bioinformatic and statistical methods, including differential expression analysis, gene-set analysis, and metabolic network analysis, were used to characterize the different myocytes.ResultsWe found that the transcriptional program associated with obesity alone was strikingly similar to that induced specifically by T2D. We identified a candidate epigenetic mechanism, H3K27me3 histone methylation, mediating these transcriptional signatures. T2D and obesity were independently associated with dysregulated myogenesis, down-regulated muscle function, and up-regulation of inflammation and extracellular matrix components. Metabolic network analysis identified that in T2D but not obesity a specific metabolite subnetwork involved in sphingolipid metabolism was transcriptionally regulated.ConclusionsOur findings identify inherent characteristics in myocytes, as a memory of the in vivo phenotype, without the influence from a diabetic or obese extracellular environment, highlighting their importance in the development of T2D.Electronic supplementary materialThe online version of this article (doi:10.1186/s13073-017-0432-2) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Type 2 diabetes and obesity induce similar transcriptional reprogramming in human myocytes

et al. 2017

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“…It is even possible that multinucleated myofibers contribute to ECM production in normal muscle. Myogenic cells secrete collagen, 94 MMP-2, 69 and decorin 95 in culture, and embryonic myoblasts secrete collagens prior to fusion, 96 but fibroblasts appear to be necessary to organize these ECM components into a functional matrix. 92,97 Fibroblasts are sensitive to mechanical loading and convert mechanical signals into altered gene expression (see review 98 ).…”

Section: Ecm Mechanicsmentioning

confidence: 99%

Structure and function of the skeletal muscle extracellular matrix

Gillies¹,

Lieber²

2011

Muscle and Nerve

768

686

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The skeletal muscle extracellular matrix (ECM) plays an important role in muscle fiber force transmission, maintenance, and repair. In both injured and diseased states, ECM adapts dramatically, a property thathas clinical manifestations and alters muscle function. Here, we review the structure, composition, and mechanical properties of skeletal muscle ECM, describe the cells that contribute to the maintenance of the ECM and, finally, overview changes that occur with pathology. New scanning electron micrographs of ECM structure are also presented with hypotheses about ECM structure-function relationships. Detailed structure-function relationships of the ECM have yet to be defined and, as a result, we propose areas for future studies.

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“…An interesting case is that of collagen 1A1 RNA (COL1A1), previously shown to consistently associate with one of the largest SC-35 domains in fibroblast nuclei, a cell-type in which it is highly expressed (Xing et al, 1995). Because this gene is also expressed in myoblasts but downregulated to low or negligible levels after cells fuse to form postmitotic skeletal muscle (Beach et al, 1985), it was interesting to determine whether the gene would remain associated with an SC-35 domains. The myotube nuclei exhibited RNA foci much smaller in developing muscle fibers than in fibroblasts.…”

Section: Localization Of Muscle-specific and Nonmuscle-specific Sequementioning

confidence: 99%

Repositioning of Muscle-specific Genes Relative to the Periphery of SC-35 Domains during Skeletal Myogenesis

Moen

Johnson

Byron

et al. 2004

MBoC

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Previous studies have shown that in a given cell type, certain active genes associate with SC-35 domains, nuclear regions rich in RNA metabolic factors and excluded from heterochromatin. This organization is not seen for all active genes; therefore, it is important to determine whether and when this locus-specific organization arises during development and differentiation of specific cell types. Here, we investigate whether gene organization relative to SC-35 domains is cell type specific by following several muscle and nonmuscle genes in human fibroblasts, committed but proliferative myoblasts, and terminally differentiated muscle. Although no change was seen for other loci, two muscle genes (Human ␤-cardiac myosin heavy chain and myogenin) became localized to the periphery of an SC-35 domain in terminally differentiated muscle nuclei, but not in proliferative myoblasts or in fibroblasts. There was no apparent change in gene localization relative to either the chromosome territory or the heterochromatic compartment; thus, the gene repositioning seemed to occur specifically with respect to SC-35 domains. This gene relocation adjacent to a prominent SC-35 domain was recapitulated in mouse 3T3 cells induced into myogenesis by introduction of MyoD. Results demonstrate a cell typespecific reorganization of specific developmentally regulated loci relative to large domains of RNA metabolic factors, which may facilitate developmental regulation of genome expression.

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Extracellular-matrix synthesis by skeletal muscle in culture. Major secreted collagenous proteins of clonal myoblasts

Cited by 16 publications

References 51 publications

Type 2 diabetes and obesity induce similar transcriptional reprogramming in human myocytes

Type 2 diabetes and obesity induce similar transcriptional reprogramming in human myocytes

Structure and function of the skeletal muscle extracellular matrix

Repositioning of Muscle-specific Genes Relative to the Periphery of SC-35 Domains during Skeletal Myogenesis

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