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PubMed2004

Pax genes in myogenesis: alternate transcripts add complexity.

Pax3 and Pax7 are powerful myogenic inducers and hence play a critical role in skeletal muscle development and regeneration. In this paper we discuss the role of Pax3 and Pax7 in dorsal patterning of the somite with subsequent determination of myogenic precursor cells for muscle formation within the developing embryo and in adult muscle. Recent evidence of the ability of stem cells to contribute to muscle regeneration in adult tissues, and the role of Pax7 in conversion of multipotent stem cells to the myogenic lineage are also discussed. Several tissue specific Pax7 transcripts that encode isoforms with different DNA binding characteristics and potentially distinct transactivation specificities are identified. The expression of a range of transcripts in the determination of different tissue lineages and distinct cell populations both in the embryo and in the adult indicates an extraordinary level of complexity. A detailed understanding of these molecules and their functions during embryogenesis and adult muscle formation is imperative for future stem cell therapies.

Alternative Splicing↗
PubMed1988

Hormonal control of myosin heavy chain genes during development of skeletal muscles.

A pattern of myosin heavy chain (MHC) switching is a hallmark of developing muscles. Factors responsible for these changes in gene expression include endogenous signals, motoneurons and hormones, especially thyroid hormones. After perturbing the innervation and/or thyroid hormone levels we have examined the neonatal-IIb MHC transition during rat development. First, denervation does not qualitatively affect the transition at either the transcriptional or translational level. Second, hypothyroidism prevents the appearance of IIb MHC and its mRNA in the innervated limb; in the denervated hypothyroid limb IIb MHC is synthesized at moderately high levels. Third, hyperthyroidism causes a precocious increase in IIb MHC in both innervated and denervated muscles. These results suggest that the transition from neonatal to adult IIb myosin synthesis is endogenously programmed during development, but is closely orchestrated by the changing neuronal and hormonal status of the animal. Thyroid hormone may exert its influence by effects both on the muscle fibre and on the developing motoneuron. In the guinea-pig the temporalis muscle is sexually dimorphic: it contains a fast-red MHC in the female but a fast-white MHC in the male. This dimorphism has been shown to be mediated by testosterone, since the castrated male synthesizes the fast-red MHC while the testosterone-supplemented female contains the fast-white MHC. During development male and female muscles initially synthesize the fast-red isoform. The male switches to the fast-white form at puberty.

Animals↗
PubMed2002

Muscle power development during the first year of life predicts neuromotor behaviour at 7 years in preterm born high-risk infants.

The aim of the study was to find if neurological function during the first year of life could predict neuromotor behaviour at 7 years of age in children born preterm with a high risk. A follow-up study of neuromotor behaviour in 52 children at a mean age of 3, 6, 12 months (corrected age) and 7 years was performed. All children were born with a gestational age less than 32 weeks and/or a birthweight under 1500 g and the infants were categorised according to their medical history in the three highest categories of the 'Neonatal Medical Index' (NMI, from category I to V, from few to serious complications). In addition, neonatal cerebral ultrasound abnormalities were used to divide the infants further into the different NMI categories. At 3 and 6 months, the relationship between active and passive muscle power was measured in shoulders, trunk and legs and (a)symmetry between right and left was noted. The results at 3 and 6 months were ranged from 1 for optimal to 5 for poor muscle power regulation. At 12 months of age, a neurological examination was done with special emphasis on the assessment of postural control, spontaneous motility, hand function and elicited infantile reactions with special attention to (a)symmetry. Outcome at 12 months was expressed as percentage of the optimal score on each subcategory. At 7 years, the motor behaviour study based on Touwen's examination for minor neurological dysfunction was performed. This investigation focuses on different functions, such as hand function, quality of walking, posture, passive muscle tone, coordination and diadochokinesis. The outcome was expressed as percentage of the optimal score on the combined subcategories. The best prediction of neuromotor behaviour at 7 years was assessed with stepwise linear multiple regression, using as potential predictors perinatal factors and outcome of motor behaviour at the corrected age of 3, 6 and 12 months. At 7 years none of the children scored 100% on the combined subcategories, 15 children (29%) scored between 75% and 99%, whereas 15 children scored less than 50%. Neuromotor behaviour at 7 years could be predicted by the NMI categorisation and gender with a sensitivity of 92% (specificity 47%; positive and negative predictive value 81% and 70%). No direct relation was found between neuromotor behaviour and cerebral ultrasound classification only, days on the ventilator and/or continuous positive airway pressure, birthweight, gestational age and dysmaturity. The best predictor of neuromotor behaviour at 7 years was the combination of outcome of muscle power in shoulders and legs at 3 months and postural control at 12 months, taking into account the gender of the child (sensitivity 95%; specificity 40%; positive predictive value 80%; negative predictive value 75%).

Birth Weight↗
PubMed1992

3,5,3'-Triiodothyronine positively regulates both MyoD1 gene transcription and terminal differentiation in C2 myoblasts.

Thyroid hormones are among the positive regulators of muscle development in vivo, but little is known about the way they work. We demonstrate here that MyoD1, one of the master genes controlling myogenesis, is a target of T3. After proliferating C2 myoblasts have been treated with T3 for 15 h, we observed a rise in MyoD1 expression at both the mRNA and protein levels. This is the first positive hormonal control of MyoD1 gene expression reported so far. We also provide data which suggest that T3 nuclear receptor(s) have a direct role on MyoD1 gene transcription: 1) C2 cells express the alpha 1 form of T3 nuclear receptors; 2) T3 up-regulates MyoD1 gene transcription and does not affect MyoD1 mRNA stability, as demonstrated by run-on and actinomycin D chase experiments, respectively; and 3) this transcriptional activation does not need the synthesis of intermediate protein(s) since it is not abolished by simultaneous treatment with cycloheximide. Moreover, in presence of T3, the increase of MyoD1 transcripts is associated with a faster terminal differentiation. Indeed we observed an earlier expression of various markers of myogenesis including myogenin (a regulatory gene of the MyoD1 family mainly involved in the triggering of terminal differentiation), myosin light chain 1A, and troponin T in T3-treated cells vs. untreated cells. We suggest that the regulation of a pivotal myogenic gene could be an important step in the control exerted by T3 on muscle development in vivo.

Animals↗
PubMed1998

Early development of EMG localized muscle fatigue in hand muscles of patients with chronic heart failure.

BACKGROUND: Patients with chronic heart failure (CHF) frequently complain of fatigue and exercise intolerance that are not directly related to the severity of cardiac failure. A not well-defined muscle function impairment is generally considered the cause of such symptoms. The frequency compression of electromyographic (EMG) signal power spectrum during isometric contractions is commonly accepted as an index of the fatigue occurring in the muscle (localized muscle fatigue). PURPOSE AND METHODS: The purpose of the study was to evaluate muscle fatigue development in a selected group of CHF patients by studying the compression of the EMG signal power spectrum. The first dorsal interosseus of the right, dominant hand was investigated at two levels of contraction: 40% and 80% of the maximal voluntary contraction (MVC). RESULTS: In CHF patients there was early development of localized muscle fatigue during the high level of contraction (80% of MVC). CONCLUSION: This study demonstrates the presence of an early development of localized muscle fatigue in CHF patients and confirms the possibility of an increased glycolytic metabolism. Moreover, the changes seem to show that muscle impairment is not limited to large muscles, but also occurs in small muscles of the hands, frequently used during daily activities. Finally, this study confirms the validity of EMG spectral analysis techniques in evaluating muscle fatigue of CHF patients, suggesting a possible use in the rehabilitation of such patients when the technique is correctly used.

Adult↗
PubMedDate not supplied

[Directions in the development of postsynaptic nondepolarizing muscle relaxants with rapidly developing action].

The experiments on unconscious cats have shown that the myoparalytic effect of postsynaptic non-depolarizing myorelaxants which have a trimethylammonium cationic group develops more rapidly than that of their triethylammonium analogues. The compound IEM-1213 is given as an example of a trimethylammonium derivative with the rigid structure of the molecule having an unusual rapidly developed effect.

Action Potentials↗
PubMed1995

Myosin light chain 3F regulatory sequences confer regionalized cardiac and skeletal muscle expression in transgenic mice.

The myosin light chain IF/3F locus contains two independent promoters, MLC1F and MLC3F, which are differentially activated during skeletal muscle development. Transcription at this locus is regulated by a 3' skeletal muscle enhancer element, which directs correct temporal and tissue-specific expression from the MLC1F promoter in transgenic mice. To investigate the role of this enhancer in regulation of the MLC3F promoter in vivo, we have analyzed reporter gene expression in transgenic mice containing lacZ under transcriptional control of the mouse MLC3F promoter and 3' enhancer element. Our results show that these regulatory elements direct strong expression of lacZ in skeletal muscle; the transgene, however, is activated 4-5 d before the endogenous MLC3F promoter, at the time of initiation of MLC1F transcription. In adult mice, transgene activity is downregulated in muscles that have reduced contributions of type IIB fibers (soleus and diaphragm). The rostrocaudal positional gradient of transgene expression documented for MLC1F transgenic mice (Donoghue, M., J. P. Merlie, N. Rosenthal, and J. R. Sanes. 1991. Proc. Natl. Acad. Sci. USA. 88:5847-5851) is not seen in MLC3F transgenic mice. Although MLC3F was previously thought to be restricted to skeletal striated muscle, the MLC3F-lacZ transgene is expressed in cardiac muscle from 7.5 d of development in a spatially restricted manner in the atria and left ventricular compartments, suggesting that transcriptional differences exist between cardiomyocytes in left and right compartments of the heart. We show here that transgene-directed expression of the MLC3F promoter reflects low level expression of endogenous MLC3F transcripts in the mouse heart.

Animals↗
PubMed2001

Two myogenin-related genes are differentially expressed in Xenopus laevis myogenesis and differ in their ability to transactivate muscle structural genes.

Among the myogenic regulatory factors, myogenin is a transcriptional activator situated at a crucial position for terminal differentiation in muscle development. It is unclear at present whether myogenin exhibits unique specificities to transactivate late muscular markers. During Xenopus development, the accumulation of myogenin mRNA is restricted to secondary myogenesis, at the onset of the appearance of adult isoforms of beta-tropomyosin and myosin heavy chain. To determine the role of myogenin in the isoform switch of these contractile proteins, we characterized and directly compared the functional properties of myogenin with other myogenic regulatory factors in Xenopus embryos. Two distinct cDNAs related to myogenin, XmyogU1 and XmyogU2, were differentially expressed during myogenesis and in adult tissues, in which they preferentially accumulated in oxidative myofibers. Animal cap assays in Xenopus embryos revealed that myogenin, but not the other myogenic regulatory factors, induced expression of embryonic/larval isoforms of the beta-tropomyosin and myosin heavy chain genes. Only XmyogU1 induced expression of the adult fast isoform of the myosin heavy chain gene. This is the first demonstration of a specific transactivation of one set of muscle structural genes by myogenin.

Amino Acid Sequence↗
PubMed1999

Expression of the alpha 6A integrin splice variant in developing mouse embryonic stem cell aggregates and correlation with cardiac muscle differentiation.

Mouse embryonic stem (ES) cells grown in aggregates give rise to several different cell types, including cardiac muscle. Given the lack of cardiac muscle cell lines, ES cells can be a useful tool in the study of cardiac muscle differentiation. The laminin-binding integrin alpha 6 beta 1 exists in two different splice variant forms of the alpha chain (alpha 6A and alpha 6B), the alpha 6A form having been implicated as possibly playing a role in cardiac muscle development, based on its distribution pattern [4, 53]. In this study we characterise the ES cell model system in terms of the expression of the two different alpha 6 splice variants. We correlate their expression with that of muscle markers and the transcription factor GATA-4, using the reverse transcription-polymerase chain reaction (RT-PCR). We confirm that alpha 6B is constitutively expressed by ES cells. In contrast, alpha 6A expression appears later and overlaps in time with a period when the muscle marker myosin light chain-2V (MLC-2V) is expressed, but no MyoD is present, which indicates the presence of cardiac muscle cells in the aggregates. We further show that GATA-4 is present at the same time. Culturing the aggregates under conditions that stimulate (transforming growth factor beta 1 supplement) or inhibit (TGF beta 1 plus 10(-9) M retinoic acid supplement) cardiac muscle differentiation does not lead to any qualitative differences in the timing of expression of these genes, but quantitative changes cannot be excluded. The TGF beta 1 supplement does, however, lead to a relatively greater expression of alpha 6A compared to alpha 6B than the TGF beta 1 plus 10(-9) M RA supplement after 6 days in culture, suggesting that alpha 6A expression is favoured under conditions that stimulate cardiac muscle differentiation. The switch towards alpha 6A expression in ES cell aggregates is paralleled by expression of the binding receptor for TGF beta (T beta RII). Stable expression of a mutated (dominant negative) T beta RII in ES cells, however, still resulted in (TGF beta-independent) upregulation of alpha 6A, demonstrating that these events were not causally related and that parallel or alternative regulatory pathways exist. The initial characterisation of differentiating ES cell aggregates in terms of alpha 6A integrin subunit expression suggests that this model system could be a valuable tool in the study of the role of the alpha 6A beta 1 integrin in cardiac muscle differentiation.

Animals↗
PubMed1997

Altered expression of the alpha7beta1 integrin in human and murine muscular dystrophies.

The alpha7beta1 integrin is the primary laminin receptor on skeletal myoblasts and adult myofibers. It has distinct functions during muscle development and contributes to muscle structural integrity. We have studied this integrin in cases where expression of dystrophin or laminin are compromised. Immunofluorescence demonstrates an increase in alpha7beta1 in patients with Duchenne muscular dystrophy and in mdx mice that lack dystrophin. Analysis of RNA from mdx mice and from patients with Duchenne and Becker muscular dystrophies indicates that the increase in the alpha7beta1 integrin is regulated at the level of alpha7 gene transcription. In contrast, the levels of alpha7beta1 integrin are severely diminished in patients with laminin alpha2 chain congenital dystrophy muscular dystrophy and in dy/dy mice that also do not make the alpha2 laminin chain. Analysis of RNA from the hindlimbs of dy/dy mice demonstrated that in the absence of laminin alpha7 gene transcription is inhibited and limited to specific alternatively spliced isoforms. We suggest that the increased expression of alpha7beta1 integrin in the absence of dystrophin compensates for the reduced dystrophin-mediated linkage of fibers with the basal lamina and modulates the development of pathology associated with these diseases. The decrease in alpha7beta1 integrin and its transcripts in the absence of laminin likely contributes to the severe myopathy that results from laminin alpha2 chain deficiency and suggests that laminin-2 regulates expression of the alpha7 integrin gene. The role of the alpha7beta1 integrin in muscle integrity also suggests that compromised expression of this receptor may underlie as yet undefined myopathies.

Adult↗
PubMed1993

Comparison of the proliferation and differentiation of myogenic satellite cells derived from Merriam's and commercial varieties of turkeys.

1. Myogenic satellite cells were isolated and cloned from the Pectoralis major muscles of 6-week-old Nicholas and Merriam's tom turkeys to compare in vitro properties of muscle development between turkeys with markedly different growth rates. 2. Although only small differences (P < or = 0.05) were noted between proliferation rates of the two cell populations in McCoy's 5A medium-15% chicken serum, satellite cells derived from the Nicholas variety were more responsive (P < or = 0.05) to mitogenic stimuli from serum at all levels tested. 3. When satellite cells were stimulated by low serum levels to differentiate into multinucleated myotubes, cells from the Merriam's turkey fused more rapidly (P < or = 0.05).

Animals↗
PubMed1992

Growth and development of human muscle: a quantitative morphological study of whole vastus lateralis from childhood to adult age.

The mechanisms underlying the increase in volume of muscle tissue, and the functional development of muscle fibers from childhood through adolescence to adult age, have been studied. Cross sections of autopsied whole vastus lateralis muscle from 22 previously physically healthy males, 5 to 37 years of age, were prepared enzyme histochemically (myofibrillar ATPase) and examined morphometrically. The data obtained on muscle cross-sectional area, size, total number, and proportion of type 1 (slow-twitch) and type 2 (fast-twitch) fibers were analyzed using linear regression techniques. The results show that the increase in muscle cross-sectional area from childhood to adult age is caused by an increase in mean fiber size. This is accompanied by a functional development of the fiber population: the proportion of type 2 fibers increases significantly from the age of 5 (approx. 35%) to the age of 20 (approx. 50%), which, in the absence of any discernible effect on the total number of fibers, is most likely caused by a transformation of type 1 to type 2 fibers.

Adolescent↗
PubMed2001

Oxygen-mediated regulation of skeletal muscle satellite cell proliferation and adipogenesis in culture.

Major problems in stem cell biology revolve around defining the developmental potential of cell populations and understanding how their potential is maintained or progressively restricted. Oxygen (O(2)) is an obvious environmental factor which has received little attention in culturing skeletal muscle progenitor cells. In this work, we examine the effects of O(2) levels on the developmental potential, proliferative capacity, and phenotype of the adult skeletal muscle fiber progenitor population (satellite cells), and cell lines that model multipotential embryonic paraxial mesoderm from which skeletal muscle develops. Both satellite cell proliferation and survival of mature fibers increased in physiologic (6%) O(2) vs. non-physiologic 20% O(2) used in virtually all traditional cell culture. Six percent O(2) conditions also accelerated the up-regulation of multiple MyoD family myogenic regulatory factors (MRFs). An unexpected finding was that fiber-adherent satellite cells could assume a non-myogenic phenotype. By the criteria of molecular markers and gross lipid accumulation, satellite cells were found to assume an adipocyte phenotype, and did so more prominently in 20% O(2) than in physiologic O(2). Selection of the adipogenic fate and execution of adipogenesis by multipotential mesenchymal cell lines was also dramatically higher in traditional 20 vs. 6% O(2), and decreased adipogenesis in physiologic O(2) was associated with significantly less expression of the adipogenic regulator, PPAR gamma. These results suggest that regulatory pathways affected by O(2) are important for satellite cell proliferation, execution of cell fate, and parent muscle survival in culture, and so may play a role in vivo under normal or pathologic conditions.

Adipocytes↗
PubMed1982

[Effect of stimulation of the head of the caudate nucleus on the activity of posture muscles during development of the instrumental avoidance reflex].

In chronic experiments on dags, instrumental avoidance reflexes associated with maintenance of a certain posture, revealed prevalence of inhibitory effect of preliminary low--frequency (2/ sec) stimulation of caudate nucleus' head in the right as well as left hemisphere on electromyographic and mechanographic components of the reflex actualizing its motor program. The most dramatic changes occurred in the posture components of the EMG which suggests the importance of the caudate nucleus' head for posture organization. The caudate nucleus' head is bilaterally involved in the pretriggering processes forerunning the instrumental reflex. At the same time, a difficulty in inhibition of resolving the instrumental task proper--avoidance of the electric current--was obvious in stimulation of the caudate nucleus' head in the system of instrumental avoidance reflexes.

Animals↗
PubMed2004

Calcium-dependent facilitation and graded deactivation of store-operated calcium entry in fetal skeletal muscle.

Activation of store-operated Ca(2+) entry (SOCE) into the cytoplasm requires retrograde signaling from the intracellular Ca(2+) release machinery, a process that involves an intimate interaction between protein components on the intracellular and cell surface membranes. The cellular machinery that governs the Ca(2+) movement in muscle cells is developmentally regulated, reflecting maturation of the junctional membrane structure as well as coordinated expression of related Ca(2+) signaling molecules. Here we demonstrate the existence of SOCE in freshly isolated skeletal muscle cells obtained from embryonic days 15 and 16 of the mouse embryo, a critical stage of muscle development. SOCE in the fetal muscle deactivates incrementally with the uptake of Ca(2+) into the sarcoplasmic reticulum (SR). A novel Ca(2+)-dependent facilitation of SOCE is observed in cells transiently exposed to high cytosolic Ca(2+). Our data suggest that cytosolic Ca(2+) can facilitate SOCE whereas SR luminal Ca(2+) can deactivate SOCE in the fetal skeletal muscle. This cooperative mechanism of SOCE regulation by Ca(2+) ions not only enables tight control of SOCE by the SR membrane, but also provides an efficient mechanism of extracellular Ca(2+) entry in response to physiological demand. Such Ca(2+) signaling mechanism would likely contribute to contraction and development of the fetal skeletal muscle.

Animals↗
PubMed1993

Evidence for myoblast-extrinsic regulation of slow myosin heavy chain expression during muscle fiber formation in embryonic development.

Vertebrate muscles are composed of an array of diverse fast and slow fiber types with different contractile properties. Differences among fibers in fast and slow MyHC expression could be due to extrinsic factors that act on the differentiated myofibers. Alternatively, the mononucleate myoblasts that fuse to form multinucleated muscle fibers could differ intrinsically due to lineage. To distinguish between these possibilities, we determined whether the changes in proportion of slow fibers were attributable to inherent differences in myoblasts. The proportion of fibers expressing slow myosin heavy chain (MyHC) was found to change markedly with time during embryonic and fetal human limb development. During the first trimester, a maximum of 75% of fibers expressed slow MyHC. Thereafter, new fibers formed which did not express this MyHC, so that the proportion of fibers expressing slow MyHC dropped to approximately 3% of the total by midgestation. Several weeks later, a subset of the new fibers began to express slow MyHC and from week 30 of gestation through adulthood, approximately 50% of fibers were slow. However, each myoblast clone (n = 2,119) derived from muscle tissues at six stages of human development (weeks 7, 9, 16, and 22 of gestation, 2 mo after birth and adult) expressed slow MyHC upon differentiation. We conclude from these results that the control of slow MyHC expression in vivo during muscle fiber formation in embryonic development is largely extrinsic to the myoblast. By contrast, human myoblast clones from the same samples differed in their expression of embryonic and neonatal MyHCs, in agreement with studies in other species, and this difference was shown to be stably heritable. Even after 25 population doublings in tissue culture, embryonic stage myoblasts did not give rise to myoblasts capable of expressing MyHCs typical of neonatal stages, indicating that stage-specific differences are not under the control of a division dependent mechanism, or intrinsic "clock." Taken together, these results suggest that, unlike embryonic and neonatal MyHCs, the expression of slow MyHC in vivo at different developmental stages during gestation is not the result of commitment to a distinct myoblast lineage, but is largely determined by the environment.

Cell Differentiation↗
PubMed2003

Inhibition of p38 MAPK signaling promotes late stages of myogenesis.

Signaling through the p38 mitogen-activated protein kinases (MAPKs) is essential for cartilage formation in primary cultures of limb mesenchyme. Here we show that, concurrent with a decrease in chondrogenesis, inhibition of p38 in limb bud cultures dramatically promotes muscle development. Specifically, treatment of primary limb bud cultures with p38 inhibitors increases the expression of myogenic markers and causes a striking increase in formation of myotubes, which were detected using antibodies specific for myosin heavy chain. These results are surprising in that they contrast with several previous reports describing a requirement for p38 during myogenesis. Nonetheless, the enhanced myogenesis leads to the formation of an extensive network of contractile myofibers, and this enhanced myogenesis can be conferred upon myogenic cells from clonal populations, such as G8 or C2C12 cells, if they are co-cultured with the limb mesenchymal cells. We provide evidence for the maintenance and rapid organization of existing, somitic-derived limb myoblasts in response to p38 inhibitors. These findings imply a novel and unexpected role for p38 MAPK inhibition in myogenesis and highlight the importance of the limb bud microenvironment in promoting the progression of limb myoblasts.

Animals↗
PubMed2004

Calcium transients regulate patterned actin assembly during myofibrillogenesis.

The highly ordered arrangement of sarcomeric myosin during striated muscle development requires spontaneous calcium (Ca(2+)) transients. Here, we show that blocking transients also compromises patterned assembly of actin thin filaments, titin, and capZ. Because a conserved temporal assembly pattern has been described for these proteins, selective inhibitors of either thick or thin filament formation were used to determine their relative temporal interdependencies. For example, inhibition of myosin light chain kinase (MLCK) by application of a specific inhibitory peptide or phorbol myistate acetate (PMA) disrupts myosin assembly without significantly affecting formation of actin bands. The MLCK inhibitor ML-7, however, disrupted actin as well as myosin. Surprisingly, agents that interfere with actin dynamics, such as cytochalasin D, produced only minor organizational disruptions in actin, capZ, and titin staining. However, cytochalasin D and other actin disrupting compounds significantly perturbed myosin organization. The results indicate that (1) Ca(2+) transients regulate one or more of the earliest steps in sarcomere formation, (2) mature actin filaments can assemble independently of myosin band formation, and (3) myosin thick filament assembly is extremely sensitive to disruption of either the actin or titin filament systems.

Actin Cytoskeleton↗