The Muscle Satellite Cell: A Review

Campion, D. R.

doi:10.1016/s0074-7696(08)62444-4

Cited by 438 publications

(223 citation statements)

References 127 publications

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“…Skeletal myoblasts are mononucleated precursor cells of skeletal muscle cells [12] that can fuse with different muscle fibre types and adopt their phenotype [12,13]. As skeletal muscles form approximately 30% to 50% of total body weight [14], we hypothesised that fusion of transplanted hSkMs from non-diabetic donors with host skeletal muscles of type 2 diabetes mellitus recipients could improve insulin sensitivity and glucose tolerance.…”

Section: Introductionmentioning

confidence: 99%

Skeletal myoblast transplantation for attenuation of hyperglycaemia, hyperinsulinaemia and glucose intolerance in a mouse model of type 2 diabetes mellitus

Lee

et al. 2009

Diabetologia

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Aims/hypothesis We aimed to demonstrate the feasibility and efficacy of intra-muscular transplantation of human skeletal myoblasts (hSkMs) for attenuation of hyperglycaemia and improvement of insulin sensitivity using a mouse model of type 2 diabetes mellitus. Methods KK Cg-Ay/J mice, aged 12 to 14 weeks, underwent an initial intraperitoneal glucose tolerance test (GTT) and were divided into the following groups: KK control group, basal medium (M199) only; KK myoblast group, with hSkM transplantation; KK fibroblast group, with human fibroblast transplantation. Non-diabetic C57BL mice were used as an additional normal control and also had hSkM transplantation. Cells were transplanted intramuscularly into the skeletal muscles of the mice. All animals were treated with ciclosporin for 6 weeks only. HbA 1c and fasting GTT, as well as serum adiponectin, cholesterol, insulin and triacylglycerol were studied. Results Immunohistochemistry studies showed extensive survival of the transplanted hSkMs in the skeletal muscles at 12 weeks, with nuclei of the hSkMs integrated into the host muscle fibres. Repeat GTT showed a significant decrease in glucose concentrations in the KK myoblast group compared with the KK control and KK fibroblast groups. The KK myoblast group also had reduced mean HbA 1c , cholesterol, insulin and triacylglycerol, and increased adiponectin compared with the KK control and KK fibroblast groups. C57BL mice showed no change in glucose homeostasis after hSkM transplant.

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Section: Introductionmentioning

confidence: 99%

Skeletal myoblast transplantation for attenuation of hyperglycaemia, hyperinsulinaemia and glucose intolerance in a mouse model of type 2 diabetes mellitus

Lee

et al. 2009

Diabetologia

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“…Varieties of muscle fibers exist and within a fiber there are major differences in gene expression between the synaptic region, the myotendinous region, and other portions of the fiber (Hall and Sanes, 1993). Satellite cells, closely associated with muscle fibers, are myoblast-like cells that add nuclei to fibers during growth and are responsible for the regenerative capacity of skeletal muscles (Campion, 1984). Despite the importance of satellite cells in skeletal muscle pathology, there is no adequate marker for them in damaged muscles (Grounds and Yablonka-Reuveni, 1993) and this has prevented rigorous examination of their behaviour.…”

Section: Introductionmentioning

confidence: 99%

MyoD protein accumulates in satellite cells and is neurally regulated in regenerating myotubes and skeletal muscle fibers

Koishi

Zhang

McLennan

et al. 1995

Developmental Dynamics

132

108

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MyoD belongs to a family of helix-loop-helix proteins that control myogenic differentiation. Transfection of various non-myogenic cell lines with MyoD transforms them into myogenic cells. In normal embryonic development MyoD is upregulated at the time when the hypaxial musculature begins to form, but its role in the function of adult muscle remains to be elucidated. In this study we examined the cellular locations of MyoD protein in normal and abnormal muscles to see whether the presence of MyoD protein is correlated with a particular cellular behaviour and to assess the usefulness of MyoD as a marker for satellite cells. Adult rats were anaesthetised and their tibialis anterior or soleus muscles either denervated, tenotomised, freeze lesioned, lesioned and denervated, or lesioned and tenotomised. At various intervals after the operations the rats were killed and their muscles removed, snap frozen, and sectioned with a cryostat along with muscles from unoperated neonatal and adult rats. The sections were processed for immunohistochemistry using a rabbit affinity-purified antibody to recombinant MyoD. MyoD proved to be an excellent marker for active satellite cells; satellite cells in neohatal and regenerating muscles contained high levels of MyoD protein. MyoD positive cells were not observed in the muscles of old adults, in which the satellite cells are fully quiescent. MyoD immunoreactivity was rapidly lost from satellite cell nuclei after they fused into myotubes and was not detected in either sub-synaptic or non-synaptic nuclei of mature fibers. Denervation, and to a lesser extent tenotomy, of lesioned muscles induced expression of MyoD in myotubal nuclei. Denervation of normal muscles also upregulated MyoD in muscle fiber nuclei, an effect which was maximal after 3 days. We conclude that MyoD protein is neurally regulated in both myotubes and muscle fibers.

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“…The third stage of differentiation is mediated by satellite cells, quiescent myogenic cells present in juvenile and adult skeletal muscles. When activated, satellite cells proliferate to produce the myoblasts needed for further growth and for the regeneration of injured muscle (Campion, 1984;Schultz et al, 1986). At each of these stages, myoblasts irreversibly exit from the cell cycle prior to differenti-0 1993 WILEY-LISS.…”

Section: Introductionmentioning

confidence: 99%

Identification of a program of contractile protein gene expression initiated upon skeletal muscle differentiation

Sutherland

Esser

Elsom

et al. 1993

Developmental Dynamics

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The functional diversity of skeletal muscle is largely determined by the combinations of contractile protein isoforms that are expressed in different fibers. Just how the developmental expression of this large array of genes is regulated to give functional phenotypes is thus of great interest. In the present study, we perform a comprehensive analysis of contractile protein isoform mRNA profiles in skeletal muscle systems representing each generation of fiber formed: primary, secondary, and regenerating fibers. We find that in each system examined there is a common pattern of isoform gene expression during early differentiation for 5 of the 6 gene families we have investigated: myosin light chain (MLCI1, MLC2, tropomyosin, troponin (Tn)C, and TnI. We suggest that the common isoform patterns observed together represent a genetic program of skeletal muscle differentiation that is independent of the mature fiber phenotype and is found in all newly formed myotubes. Within each of these contractile protein gene families the program is independent of the isoforms of myosin heavy chain (MHC) expressed. The maintenance of such a program may reflect a specific requirement of the initial differentiation process. 0 1993 Wiley-Liss, Inc.

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The Muscle Satellite Cell: A Review

Cited by 438 publications

References 127 publications

Skeletal myoblast transplantation for attenuation of hyperglycaemia, hyperinsulinaemia and glucose intolerance in a mouse model of type 2 diabetes mellitus

Skeletal myoblast transplantation for attenuation of hyperglycaemia, hyperinsulinaemia and glucose intolerance in a mouse model of type 2 diabetes mellitus

MyoD protein accumulates in satellite cells and is neurally regulated in regenerating myotubes and skeletal muscle fibers

Identification of a program of contractile protein gene expression initiated upon skeletal muscle differentiation

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