Composition of newly forming motor units in prenatal rat intercostal muscle

Sheard, Philip W.; Duxson, Marilyn J.

doi:10.1002/(sici)1097-0177(199602)205:2<196::aid-aja10>3.0.co;2-6

Cited by 8 publications

(3 citation statements)

References 67 publications

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“…Unlike fiber type plasticity, which is primarily regulated by slow and fast type firing patterns of motor neurons, initial fiber type specification during embryonic muscle development is initiated without significant input from motor neurons [181]. Nerve input gains control over muscle fiber type development only in later fetal stages [182]. To support the presence of nerve-independent mechanisms of fiber type specification, it has been shown that calcineurin, one of the main nerve activity-dependent regulators of slow fiber gene expression in adult muscle, is dispensable for the development of slow type fibers in embryonic skeletal muscle [183].…”

Section: Developmental Regulation Of Skeletal Muscle Fiber Typementioning

confidence: 99%

Genetic Dissection of the Physiological Role of Skeletal Muscle in Metabolic Syndrome

Hagiwara

2014

New Journal of Science

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The primary deficiency underlying metabolic syndrome is insulin resistance, in which insulin-responsive peripheral tissues fail to maintain glucose homeostasis. Because skeletal muscle is the major site for insulin-induced glucose uptake, impairments in skeletal muscle’s insulin responsiveness play a major role in the development of insulin resistance and type 2 diabetes. For example, skeletal muscle of type 2 diabetes patients and their offspring exhibit reduced ratios of slow oxidative muscle. These observations suggest the possibility of applying muscle remodeling to recover insulin sensitivity in metabolic syndrome. Skeletal muscle is highly adaptive to external stimulations such as exercise; however, in practice it is often not practical or possible to enforce the necessary intensity to obtain measurable benefits to the metabolic syndrome patient population. Therefore, identifying molecular targets for inducing muscle remodeling would provide new approaches to treat metabolic syndrome. In this review, the physiological properties of skeletal muscle, genetic analysis of metabolic syndrome in human populations and model organisms, and genetically engineered mouse models will be discussed in regard to the prospect of applying skeletal muscle remodeling as possible therapy for metabolic syndrome.

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Section: Developmental Regulation Of Skeletal Muscle Fiber Typementioning

confidence: 99%

Genetic Dissection of the Physiological Role of Skeletal Muscle in Metabolic Syndrome

Hagiwara

2014

New Journal of Science

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“…Primary and secondary myotubes were quantified by counting slow MHC-positive (primary) and slow MHC-negative (secondary) myotubes Sheard and Duxson, 1996). Consecutive sections were labelled with the MY32 antibody, which stains all myotubes at E18.5.…”

Section: Myotube Quantificationmentioning

confidence: 99%

Knock-in of integrin β1D affects primary but not secondary myogenesis in mice

et al. 2003

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Integrins are extracellular matrix receptors composed of α and β subunits involved in cell adhesion, migration and signal transduction. The β1 subunit has two isoforms, β1A ubiquitously expressed and β1D restricted to striated muscle. They are not functionally equivalent. Replacement of β1A by β1D (β1D knock-in) in the mouse leads to midgestation lethality on a 50% Ola/50% FVB background [Baudoin, C., Goumans, M. J., Mummery, C. and Sonnenberg, A. (1998). Genes Dev. 12, 1202-1216]. We crossed the β1D knock-in line into a less penetrant genetic background. This led to an attenuation of the midgestation lethality and revealed a second period of lethality around birth. Midgestation death was apparently not caused by failure in cell migration, but rather by abnormal placentation. The β1D knock-in embryos that survived midgestation developed until birth, but exhibited severely reduced skeletal muscle mass. Quantification of myotube numbers showed that substitution of β1A with β1D impairs primary myogenesis with no direct effect on secondary myogenesis. Furthermore, long-term primary myotube survival was affected in β1D knock-in embryos. Finally, overexpression of β1D in C2C12 cells impaired myotube formation while overexpression of β1A primarily affected myotube maturation. Together these results demonstrate for the first time distinct roles for β1 integrins in primary versus secondary myogenesis and that the β1A and β1D variants are not functionally equivalent in this process.

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“…To culture embryonic skeletal muscle in vitro, the intercostal muscles, which run as thin sheets between adjacent ribs, were chosen, because no dissection of the muscle is required and their size makes possible the diffusion of oxygen and nutrients. In addition, their development is well documented, and they play an essential role in respiratory movements 20, 30, 31. The muscles develop by the formation of primary and secondary fibers, contain a mixture of fast and slow fiber types, and show a gradation in gene expression along their rostro‐caudal axis,8, 30 The current organ culture protocol was coupled with square‐wave electroporation, a technique in which short pulses of current are passed across suspensions of cells or pieces of tissue.…”

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confidence: 99%

Gene transfer into intact fetal skeletal muscle grown in vitro

et al. 2004

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The development of an organ culture system for growing prenatal intercostal muscle in vitro and its use to study gene function is described. Fetal skeletal muscle is relatively inaccessible during the key stages of its development, and this method enables DNA transfections and other manipulations to be carried out. The system allows cell proliferation and differentiation to continue and also maintains the morphology and fiber types of developing muscle. Gene transfer into cultured embryonic intercostal muscle was achieved by square-pulse electroporation of intact pieces of tissue. Expression of a marker gene (GFP) was found within 5 h and maintained for 2 days in muscle fibers and cells. The technique should enable the function of genes implicated in muscle development and disease to be studied at stages when access is difficult and in a controlled environment.

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Composition of newly forming motor units in prenatal rat intercostal muscle

Cited by 8 publications

References 67 publications

Genetic Dissection of the Physiological Role of Skeletal Muscle in Metabolic Syndrome

Genetic Dissection of the Physiological Role of Skeletal Muscle in Metabolic Syndrome

Knock-in of integrin β1D affects primary but not secondary myogenesis in mice

Gene transfer into intact fetal skeletal muscle grown in vitro

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