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At least 127 records · Page 7Linked to original sources
PubMed1998

Patterns of superficial fibre formation in the European pearlfish (Rutilus frisii meidingeri) provide a general template for slow muscle development in teleost fish.

The debate about the pattern of muscle formation in teleost fish has recently been heightened in the literature. Here we examine superficial muscle development in the pearlfish, a cyprinid endemic to a small area of Central Europe, and uninfluenced by economic interest and breeding. Using light and electron microscopy, histochemistry and immunohistochemistry techniques, we report that: (1) Superficial fibre precursors originate close to the notochord, are part of the same cell population as the so-called muscle pioneer cells, and are transferred laterally to end up at the surface of the myotome. (2) Superficial fibre maturation is exceptionally rapid. Structural and enzymatic functionality is attained at a time when prospective deep fibres have not passed beyond the early myotube state. This strong contrast weakens as the embryo develops. (3) Apart from the muscle pioneers, the superficial fibres appear to be capable of functioning before they receive any direct innervation, implying that signals are transferred to these fibres via cell-to-cell junctions. We suggest that the capability of rapid superficial fibre maturation is a rather general feature among teleosts and may aid pre-hatch survival under a variable environment. Our results indicate that muscle formation in teleost fish may follow a common basic pattern that is open to considerable ontogenetic and phylogenetic modification in response to habitat conditions.

Animals↗
PubMed1976

Insulin action on glucose transport and calcium fluxes in developing muscle cells in vitro.

The glucose transport system of developing muscle cells in vitro is described. Uptake experiments showed stereospecificity but no saturation or competition. Km-values for early myoblasts could not be determined; with progressive development, the absolute amount of uptake increases and becomes insulin sensitive. Km-values of about 13 mM basal and 32 mM for insulin stimulation were determined and discussed with respect to the glucose transport mechanism. Basal and insulin-dependent transport were shown to be dependent on the presence of calcium in the medium. Moreover, the ionophore A 23187 could be shown to mimic the insulin effect on glucose uptake. 45Ca saturation and desaturation experiments showed that insulin enhances the "mitochondrial" calcium pool by 35% and increases the apparent "cytoplasmic" efflux rate constant by 50%. We propose that insulin increases the free cytoplasmic calcium concentration, which may be the intracellular signal for the stimulation of glucose transport.

Animals↗
PubMed1995

Synapse-associated expression of an acetylcholine receptor-inducing protein, ARIA/heregulin, and its putative receptors, ErbB2 and ErbB3, in developing mammalian muscle.

Developing motor axons induce synaptic specializations in muscle fibers, including preferential transcription of acetylcholine receptor (AChR) subunit genes by subsynaptic nuclei. One candidate nerve-derived signaling molecule is AChR-inducing activity (ARIA)/heregulin, a ligand of the erbB family of receptor tyrosine kinases. Here, we asked whether ARIA and erbB kinases are expressed in patterns compatible with their proposed signaling roles. In developing muscle, ARIA was present not only at synaptic sites, but also in extrasynaptic regions of the muscle fiber. ARIA was synthesized, rather than merely taken up, by muscle cells, as indicated by the presence of ARIA mRNA in muscle and of ARIA protein in a clonal muscle cell line. ARIA-responsive myotubes expressed both erbB2 and erbB3, but little EGFR/erbB1 or erbB4. In adults, erbB2 and erbB3 were localized to the postsynaptic membrane. ErbB3 was restricted to the postsynaptic membrane perinatally, at a time when ARIA was still broadly distributed. Thus, our data are consistent with a model in which ARIA interacts with erbB kinases on the muscle cell surface to provide a local signal that induces synaptic expression of AChR genes. However, much of the ARIA is produced by muscle, not nerve, and the spatially restricted response may result from the localization of erbB kinases as well as of ARIA. Finally, we show that erbB3 is not concentrated at synaptic sites in mutant mice that lack rapsyn, a cytoskeletal protein required for AChR clustering, suggesting that pathways for synaptic AChR expression and clustering interact.

Aging↗
PubMed1987

Evidence for sequential expression of multiple AMP deaminase isoforms during skeletal muscle development.

AMP deaminase (myoadenylate deaminase; EC 3.5.4.6) is an integral part of the myofibril in skeletal muscle, and this enzyme plays an important role in energy metabolism in this tissue. We report here the identification of three AMP deaminase isoforms during skeletal muscle development in the rat. An embryonic isoform is expressed in the developing hindlimb of the rat between 7 and 14 days of gestation. This isoform is not unique to skeletal muscle or the embryo as it is also expressed in many nonmuscle tissues of the perinatal and adult rat. A perinatal isoform of AMP deaminase that is restricted to skeletal muscle is produced 4-6 days before birth and persists for 2-3 weeks of postnatal life. An adult, skeletal muscle-specific isoform of AMP deaminase appears at birth and reaches maximal levels after 3 weeks of postnatal development. We conclude from these studies there is a developmentally controlled program that leads to the sequential expression of AMP deaminase isoforms during the transition from embryonic to adult skeletal muscle.

AMP Deaminase↗
PubMed1993

Histochemical and contractile property changes during human muscle development.

When the histochemical and contractile properties of infant muscles change postnatally, and what influence muscle function has on these changes, were the focus of this study. Contractile properties were measured in the plantaflexor (PF) and dorsiflexors (DF) of 19 newborns and 36 infants aged 5-16 months. Infants were tested between one and four times at monthly intervals. Measurements included maximal twitch tension (Pt), time to peak tension (TPT), and half-relaxation times (1/2RT). TPT was similar in PF (77 ms) and DF (73 ms) at birth, remained unchanged in DF, and slowed in PF to 110-120 ms between 9 and 12 months. Type I distributions were determined at autopsy in fetal through to adult muscles. Completion of differentiation occurred in soleus at about the age that contractile properties slowed and infants started to use these muscles more. A trend of higher percentages of type I distributions was also noted in children than either newborns or adults in other muscles. The implications of these findings and the clinical use of these methods for evaluating peripheral neuromuscular function is discussed.

Adolescent↗
PubMed1992

Formation of highly organized skeletal muscle fibers in vitro. Comparison with muscle development in vivo.

Two methods were developed in which long-term cultures of quail skeletal muscle were established so that all of the muscle fibers develop in a highly oriented manner. The muscle fibers became spontaneously and vigorously contractile and established strong connections with the extracellular matrix at their ends that closely duplicate the structure of the myotendinous junction. A continuous basal lamina was formed around each muscle fiber that contained type IV collagen, laminin and heparan sulfate proteoglycan. With one of the methods, an extensive extracellular matrix developed around each muscle fiber that was highly organized with the formation of a distinctive epimysium, perimysium and endomysium. Analysis of the cultures by both methods for different isoforms of myosin showed expression of an adult form of myosin by some of the muscle cells. The results therefore demonstrate that muscle development in the present culture systems proceeds extensively for several weeks. It will now be possible to investigate directly the structure of the connections between muscle fibers and the extracellular matrix.

Animals↗
PubMed1996

Pax3 modulates expression of the c-Met receptor during limb muscle development.

Pax3 is a transcription factor whose expression has been used as a marker of myogenic precursor cells arising in the lateral somite destined to migrate to and populate the limb musculature. Accruing evidence indicates that the embryologic origins of axial and appendicular muscles are distinct, and limb muscle abnormalities in both mice and humans harboring Pax3 mutations support this distinction. The mechanisms by which Pax3 affects limb muscle development are unknown. The tyrosine kinase receptor for hepatocyte growth factor/scatter factor encoded by the c-met protooncogene is also expressed in limb muscle progenitors and, like Pax-3, is required in the mouse for limb muscle development. Here, we show that c-met expression is markedly reduced in the lateral dermomyotome of Splotch embryos lacking Pax3. We show that Pax3 can stimulate c-met expression in cultured cells, and we identify a potential Pax3 binding site in the human c-MET promoter that may contribute to direct transcriptional regulation. In addition, we have found that several cell lines derived from patients with rhabdomyosarcomas caused by a t(2;13) chromosomal translocation activating PAX3 express c-MET, whereas those rhabdomyosarcoma cell lines examined without the translocation do not. These results are consistent with a model in which Pax3 modulates c-met expression in the lateral dermomyotome, a function that is required for the appropriate migration of these myogenic precursors to the limb where the ligand for c-met (hepatocyte growth factor/scatter factor) is expressed at high levels.

Animals↗
PubMed1994

Temporal differences in the induction of dihydropyridine receptor subunits and ryanodine receptors during skeletal muscle development.

The expression of the dihydropyridine (DHP) and ryanodine receptors in skeletal muscle was investigated during development of rat myotubes in culture as well as during embryonic and postnatal development in the rat. Through the use of specific gene probes, antibodies and radioligand binding ([3H]PN 200-110 (DHP) and [3H]ryanodine), we identified a significant difference between the time course of appearance of the DHP receptor and the ryanodine receptor during muscle development. Although the number of DHP receptors dramatically increased at early stages of development (up to day 7 in tissue culture and day 20 postnatal), increase in the ryanodine receptor density occurred comparatively later at day 10 in culture and day 30 postnatal. This process was associated with parallel changes in the expression of the mRNA encoding the alpha 1, alpha 2, and beta subunits of the DHP receptor and the skeletal muscle ryanodine receptor. The genes encoding the DHP receptor subunits were activated in a temporally distinct transcript appeared and plateaued first, at the onset of myoblast fusion and day 16 embryonic. This was followed closely by an increase in expression of the mRNAs for alpha 1 and alpha 2 subunits which coincided with the sharp rise in the DHP receptor density. Ryanodine receptor gene expression was induced well after the DHP receptor gene expression had plateaued. The temporal appearance of the polypeptides comprising the DHP receptor subunits and the ryanodine receptor paralleled the induction of the genes encoding these receptors. These results imply that gene expression is a major mechanism that contributes to the regulation of DHP and ryanodine receptor numbers during muscle development. The temporal differences in the induction of the genes encoding the DHP receptor subunits and the ryanodine receptor suggests that these genes are under the control of distinct endogenous factors. These differences in expression of the DHP receptor and the ryanodine receptor may contribute to the different mechanisms of excitation-contraction coupling in immature versus adult skeletal muscle.

Animals↗
PubMed1997

Presence of laminin alpha5 chain and lack of laminin alpha1 chain during human muscle development and in muscular dystrophies.

There is currently a great interest in identifying laminin isoforms expressed in developing and regenerating skeletal muscle. Laminin alpha1 has been reported to localize to human fetal muscle and to be induced in muscular dystrophies based on immunohistochemistry with the monoclonal antibody 4C7, suggested to recognize the human laminin alpha1 chain. Nevertheless, there seems to be no expression of laminin alpha1 protein or mRNA in developing or dystrophic mouse skeletal muscle fibers. To address the discrepancy between the results obtained in developing and dystrophic human and mouse muscle we expressed the E3 domain of human laminin alpha1 chain as a recombinant protein and made antibodies specific for human laminin alpha1 chain (anti-hLN-alpha1G4/G5). We also made antibodies to the human laminin alpha5 chain purified from placenta. In the present report we show that hLN-alpha1G4/G5 antibodies react with a 400-kDa laminin alpha1 chain and that 4C7 reacts with a 380-kDa laminin alpha5 chain. Immunohistochemistry with the hLN-alpha1G4/G5 antibody and 4C7 revealed that the two antibodies stained human kidney, developing and dystrophic muscle in distinct patterns. Our data indicate that the previously reported expression patterns in developing, adult, and dystrophic human muscle tissues with 4C7 should be re-interpreted as an expression of laminin alpha5 chain. Our data are also consistent with earlier work in mouse, indicating that laminin alpha1 is largely an epithelial laminin chain not present in developing or dystrophic muscle fibers.

Adult↗
PubMed1991

Insulin-like growth factors and their receptors in muscle development.

Several proteins involved in IGF action are expressed in C2 cells and their abundance was found to vary as a function of development. IGF-I and II mRNA levels rose 10 and 25-fold, respectively, during differentiation, and were accompanied by an increase in growth factor secretion. The accumulation of IGF-II in conditioned culture medium was much greater than that of IGF-I. There was also an increase in the number of IGF-I receptors and IGF-II/CIMPR on the cell surface during differentiation. The sustained rise in IGF-II/CIMPR expression appeared to be a consequence of a similar increase in its mRNA abundance. The mechanisms responsible for the transient increment in IGF-I receptor number were not assessed, although it is likely that the decline in IGF-I receptor content after 72 hours in differentiation medium was a consequence of down-regulation by the IGF-II that accumulated in the medium (35). In contrast to the 13-fold rise in IGF-II/CIMPR mRNA levels, transcript levels for the CDMPR remained constant during C2 cell development, enzymatic activities of two lysosomal enzymes did not change, and only a small increment was detected at a single time point in the expression of several lysosomal enzyme mRNAs. In addition, during C2 muscle differentiation, a novel IGF binding protein was induced. These results demonstrate modulation of several components of IGF signaling pathways in differentiating myoblasts, and argue for a local role for IGFs in muscle development.

Animals↗
PubMed1998

Tissue-specific effects of hypothyroidism on postnatal muscle development in the barnacle goose.

The hypothesis that tissue-specific levels of thyroid hormones may be required for normal locomotor muscle development was investigated in the barnacle goose Branta leucopsis. Hypothyroidism was induced in goslings by treatment with methimazole from either 3 days or 2 weeks of age, and birds were killed at 7 weeks of age. The masses of the pectoralis, iliofibularis, semimembranosus and cardiac ventricle muscles were measured, and samples from these tissues were analysed for the mass-specific activity of the mitochondrial enzyme citrate synthase (CS). An ultrastructural electron micrograph analysis of the pectoralis was also carried out. No significant differences were found between the two hypothyroid groups except for the effect on the relative mass of the iliofibularis muscle. Developmental responses to hypothyroidism were found to be tissue-specific. Hypothyroidism resulted in a significantly lower relative cardiac ventricle mass (by 17 %) and CS activity of the leg muscles (by 34 %), while absolute leg muscle mass was not affected. The relative mass of the pectoralis was significantly lower (by 57 %) in hypothyroid birds and showed a significant, uniformly lower CS activity (by 60-83 %) as a result of a lower mitochondrial fractional volume. Haematocrit and capillary-to-fibre ratio in the pectoralis were also significantly lower in hypothyroid birds, and skeletal growth and plumage development were affected.

Animals↗
PubMed1998

MyoD and MEF2A mediate activation and repression of the p75NGFR gene during muscle development.

In an effort to clarify transient expression of the NGF low-affinity receptor p75NGFR during muscle development we have focused on the molecular mechanisms involved in the initiation and cessation of p75NGFR gene expression. Using quiescent C3H10T1/2 fibroblast as a tool, we observed that induction of differentiation competence in MyoD-transfected 10T1/2 fibroblasts was accompanied by the initiation of p75NGFR expression. Moreover, we could show that the bHLH transcription factor MyoD itself is a powerful candidate for transcriptional activation of the p75NGFR gene in muscle precursor cells. By means of MyoD-mutants we have found that both the amino terminus of the MyoD molecule as well as the bHLH-region are essential for transcriptional activity on the p75NGFR promoter. The fact that myocyte enhancer factor MEF2A inactivated MyoD-induced p75NGFR promoter activity strongly suggests that cell-specific regulation of the p75NGFR gene might be strictly dependent on the intracellular composition and balance of the appropriate bHLH-transcription factors and their modulators.

Cell Differentiation↗
PubMed1987

Developing muscle spindles in the mouse masseter muscle studied by electron microscopy.

The morphogenesis of the muscle spindles of the masseter muscle was investigated by electron microscopy. The mice used in this study were those from the 16-day-old fetuses to the four-day-old young, and the three-month-old adult ICR mice. At the time of observation the formation of the masseter muscle spindle had already started in the 16-day-old fetus. In the 17-day-old fetus, the sensory nerve terminated not only in the myotube but also in the myoblast in which no myofilaments were yet formed. From the observations on the 16-day-old and 17-day-old fetuses, it is suggested that the myotubes of the intrafusal muscle fibers are formed by the fusion of the myocytes already containing the myofilaments. The gamma motor end-plate appeared two days later than the sensory nerve terminal formation in the muscle spindle. The initial inner capsule of the spindle was observed in the four-day-old young. The cell without the myofilaments appeared amidst the cluster of the intrafusal muscle fibers in the three-day-old young. It is considered that this cell may be the origin of the inner capsule cell. The periaxial space formation and the myelination of the masseteric nerve fiber occurred in the four-day-old young. The formation of the postsynaptic folds was observed in the extrafusal muscle fiber at the same stage. Thus, the muscle spindles, nerve fibers and the extrafusal muscle fibers showed a remarkable development at the same time in this early postnatal stage.

Animals↗
PubMed1988

Quantitative relationships between motoneuron and muscle development in Xenopus laevis: implications for motoneuron cell death and motor unit formation.

A common approach to the study of neural regression has been to correlate the timing of cell loss with other events such as target development. Most of these studies have areas of uncertainty. First, the analysis is normally carried out on groups of neurons that innervate a variety of targets. Second, there are some doubts about the reliability of light microscopic quantitation of muscle development. In this study, the period of cell death in the semimembranosus motor pool of Xenopus laevis has been estimated and correlated with an electron microscopic study of the development of the semimembranosus. The period of cell death of semimembranosus motoneurons was estimated on the basis of their position in the spinal cord and from the number of myelinated axons in the semimembranosus motor nerve. The semimembranosus motor pool contained approximately 70 motoneurons and was located 17-37% along the rostrocaudal axis of the lumbar cord. Cell loss from this motor pool occurred between stages 53-54 and 56, whereas cell death in the entire lumbar cord extended beyond stage 58. Primary myogenesis occurred between stages 53 and 54 in the semimembranosus. There was then a hiatus in myotube production until secondary myogenesis began around stage 56. It is concluded that secondary myotubes are not involved in regulating motoneuron cell death and that the number of primary myotube clusters is similar in magnitude to the number of motoneurons that will ultimately survive the period of cell death. The implications of these observations for theories of cell death and motor unit formation are discussed.

Aging↗
PubMed1992

Localization of mRNAs coding for CMD1, myogenin and the alpha-subunit of the acetylcholine receptor during skeletal muscle development in the chicken.

Myogenin and CMD1, the chicken homologue of MyoD, transactivate the promoter of the alpha-subunit of the acetylcholine receptor (AChR) in chicken fibroblasts. The expression of these three genes was followed by in situ hybridization. In two-day-old embryos the CMD1 gene is expressed shortly before the AChR alpha-subunit and the myogenin genes. At day 19 extrajunctional AChR mRNA clusters have disappeared and myogenin mRNAs are no longer detected in PLD muscle. Moreover, both myogenin and CMD1 mRNA levels increase after muscle denervation in chicks. These data are compatible with a role for myogenic factors in the induction and maintenance of extra-junctional expression of the AChR genes during early muscle development. Using digoxygenin labelled RNA probes, we also show that the mRNAs for the AChR alpha-subunit display a punctated, probably perinuclear distribution, whereas mRNAs for myogenic genes accumulate in the sarcoplasm around subsets of nuclei in the muscle fiber.

Animals↗
PubMed1989

Myosin light chain 3 synthesis during chick pectoralis muscle development in ovo.

The level of myosin light chain 3 (LC3) in vertebrate skeletal muscle is developmentally regulated in a tissue-specific manner. We have used the RNA-cDNA hybridization assay to quantitate LC3 mRNA levels at various stages of chick pectoralis muscle development in ovo. The LC3 mRNA was found significantly in breast muscle only on Day 16 in ovo and later, the level of mRNA ranging from about 30 to 32% of that present in adult tissue. These values are in good agreement with the corresponding levels of LC3 in embryonic muscle. These results do not support the earlier reports that the protein and mRNA for LC3 accumulate in a noncoordinate manner in embryonic pectoralis muscle and they suggest that LC3 synthesis in ovo is regulated primarily at the transcriptional level.

Animals↗