Changes in the diffusion distance in the rat heart muscle during development.
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Animals↗
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clc is co-expressed with clf or cntfr in developing mouse muscles.
BACKGROUND: The ciliary neurotrophic factor (CNTF) receptor is composed of two signalling receptor chains, gp130 and the leukaemia inhibitory factor receptor, associated with a non-signalling CNTF binding receptor alpha component (CNTFR). This tripartite receptor has been shown to play important roles in the development of motor neurons, but the identity of the relevant ligand(s) is still not clearly established. Recently, we have identified two new ligands for the CNTF receptor complex. These are heterodimeric cytokines composed of cardiotrophin-like cytokine (CLC) associated either with the soluble receptor subunit cytokine-like factor-1 (CLF) or the soluble form of the binding receptor itself (sCNTFR). RESULTS: Here we show that, during development, clc is expressed in lung, kidney, vibrissae, tooth, epithelia and muscles during the period of development corresponding to when motoneuron loss is observed in mice lacking a functional CNTF receptor. In addition, we demonstrate that it is co-expressed at the single cell level with clf and cntfr, supporting the idea that CLC might be co-secreted with either CLF or sCNTFR. CONCLUSION: This expression pattern is in favor of CLC, associated either with CLF or sCNTFR, being an important player in the signal triggered by the CNTF receptor being required for motoneuron development.
Journal Article↗
Acute lindane poisoning with development of muscle necrosis.
A 35-year-old man ingested food contaminated with lindane, an insecticide containing almost pure gamma hexachlorocyclohexane. Grand mal seizures and severe acidemia developed rapidly. The seizures recurred for nearly 2 hours, then ceased. In addition, the patient had muscle weakness and pain, headaches, episodic hypertension, myoglobinuria, acute renal failure and anemia. Pancreatitis developed 13 days after the ingestion of lindane. A muscle biopsy on the 15th day of illness demonstrated widespread necrosis and regeneration of muscle fibres. The patient's condition improved and he was discharged 24 days after the onset of his illness. During the year following the poisoning the patient noted difficulty with recent memory, loss of libido and easy fatigability. One year after lindane ingestion the results of physical examination, including those for muscle power and bulk, were normal.
Acute Disease↗
Myostatin rapid sequence evolution in ruminants predates domestication.
Myostatin (GDF-8) is a negative regulator of skeletal muscle development. This gene has previously been implicated in the double muscling phenotype in mice and cattle. A systematic analysis of myostatin sequence evolution in ruminants was performed in a phylogenetic context. The myostatin coding sequence was determined from duiker (Sylvicapra grimmia caffra), eland (Taurotragus derbianus), gaur (Bos gaurus), ibex (Capra ibex), impala (Aepyceros melampus rednilis), pronghorn (Antilocapra americana), and tahr (Hemitragus jemlahicus). Analysis of nonsynonymous to synonymous nucleotide substitution rate ratios (Ka/Ks) indicates that positive selection may have been operating on this gene during the time of divergence of Bovinae and Antilopinae, starting from approximately 23 million years ago, a period that appears to account for most of the sequence difference between myostatin in these groups. These periods of positive selective pressure on myostatin may correlate with changes in skeletal muscle mass during the same period.
Amino Acid Sequence↗
The AeAct-4 gene is expressed in the developing flight muscles of female Aedes aegypti.
Population reduction of mosquitoes is an effective method for controlling dengue fever and malaria transmission. Recent developments in control techniques include proposals to construct transgenic strains of mosquitoes carrying dominant, conditional-lethal genes under the control of sex- and stage-specific promoters. In order to identify such promoters, subtractive cDNA libraries derived from male and female pupal mRNA of the yellow fever mosquito, Aedes aegypti, were constructed and screened. A cDNA clone, F49, corresponds to a gene expressed specifically in female pupae. Sequence analyses revealed that this gene belongs to the actin gene family, and therefore was designated Aedes Actin-4 (AeAct-4). Transcription analyses demonstrated that this gene is expressed predominantly in the indirect flight muscles and, to a lesser extent, the legs of developing female mosquitoes. The promoter of this gene may be a useful tool for developing conditional lethal strains of mosquitoes.
Actins↗
Lactate and contractile force in frog muscle during development of fatigue and recovery.
The relationship between lactic acid concentration and twitch tension was reevaluated in electrically stimulated frog sartorius muscle. In muscles stimulated under anaerobic conditions at a rate of 30 stimuli/MIN CONTRACTILE FORCE DECREASED TO 36% OF THE INITIAL VALUE IN 15 MIN, Concomitantly lactate increased from 3.3 to 18.7 mumol/g of muscle. The correlaiton between the increase in lactate and the decrease in contractile force was significant (r = -0.99, P less than 0.000001). Recovery occurred in two phases. A rapid increase in contractile force, which represented 20% of the total recovery, took place during the first 15 s and occurred concomitantly with an increase in ATP from 3.9 to 4.6 mumol/g. Lactate concentration did not change significantly during this period. The second phase of recovery of contractile force was complete in 50 min. Lactate concentration and contractile force were significatly correlated during recovery (r = -0;92, P less than 0.00001). However, recovery of contractile force lagged behind the decrease in lactate; a given concentration of muscle lactate was associated with a higher contractile force early during development of fatigue than late during recovery.
Adenosine Triphosphate↗
Balancing LncRNA H19 and miR-675 Bioconversion as a Key Regulator of Embryonic Myogenesis Under Maternal Obesity.
BACKGROUND: Maternal obesity (MO) impairs fetal skeletal muscle development, but the underlying mechanisms remain poorly defined. The regulatory roles of lncRNA H19 and its first exon derived microRNA675 (miR675) in prenatal muscle development remain to be examined. H19/Igf2 are in the same imprinting cluster with H19 expressed from the maternal allele while Igf2 expresses paternally. H19 contains a G-rich loop, and KH-type splicing regulatory protein (KHSRP) mediates the biogenesis of pre-miRNAs containing G-rich loops, which depends on its phosphorylation by AKT, a key mediator of IGF2 signalling. This study aims to depict the elusive function of these regulators that are affected by MO during embryonic myogenesis. METHODS: Single-cell transcriptomic sequencing and GeoMx spatial RNA sequencing were performed to identify the differentially expressed genes between embryos from MO and control (CT) mice. Both E11.5 and E13.5 embryos were collected and analysed to validate the sequencing data. The roles of H19 and miR657 in myogenesis were further analysed in P19 embryonic cells via CRISPR/dCas9-mediated H19 activation and inhibition. The epigenetic changes of H19 were analysed by methylated DNA immunoprecipitation, and allele-targeted analysis of H19 was performed by crossing C57BL/6J and CAST/EiJ mice. RESULTS: Transcriptomic analysis showed that MO embryos contained less differentiated myocytes (1.34%) than CT embryos (2.86%). Myogenesis-related GO biological processes were down-regulated in the MO embryonic myotome region. MO embryos showed lower expression of myogenic transcription factors such as Myf5, Myod1, Myog, Mef2c and Myh3 (p < 0.05). MO altered epigenetic modifications of the H19 genomic cluster, showing a decreased methylation level in H19 imprinting control region (p < 0.05) and a diallelic expression pattern of H19, which elevated its expression in MO embryos. Overexpression of H19 inhibited myogenesis in P19 cells, but miR675 promoted myogenesis, suggesting the critical regulatory roles of bioconversion of H19 to miR675. A KHSRP mediates the biogenesis of miR675, a process that relies on its phosphorylation by IGF2/AKT signalling. Knocking-down of KHSRP and inhibition of AKT abolished miR675 biogenesis. MO suppressed IGF2/AKT signalling and blocked KHSRP-dependent miR675 biogenesis in embryos. CONCLUSIONS: We found differential effects of H19 and miR675 on embryonic myogenesis. MO up-regulates H19 but blocks its miR675 bioconversion via suppressing IGF2/AKT/KHSRP signalling axis. Myogenesis in MO embryos was impeded due to the highly accumulated H19 and blocked miR675 biogenesis.
RNA, Long Noncoding↗
Ultrastructure of developing flight muscle in Drosophila. I. Assembly of myofibrils.
In order to evaluate the effects of specific mutations on sarcomere assembly and function in vivo, we describe the course of normal development of Drosophila indirect flight muscle (IFM) in staged pupae using electron microscopy. We find that no contractile assemblies remain in larval muscle remnants invaded by imaginal myoblasts, establishing that myofibrils in IFM assemble de novo. Stress-fiber-like structures or other template structures are not prominent before or during sarcomere assembly. By 42 hr pupation (eclosion approximately 112 hr), thick and thin filaments have appeared simultaneously in slender, interdigitated arrays between regularly spaced Z-bodies. Each tiny, uniformly striated myofibril forms within a "sleeve" of microtubules, and both microtubules and myofibrils are attached to the cell membrane at each end of the fiber from the initial stages of assembly. Later in pupation, the microtubule "sleeves" disassemble. Sarcomere number appears to remain constant. We saw no evidence that terminal sarcomeres are sites for addition of new sarcomeres or that Z-lines split transversely, producing new, very short sarcomeres. Rather, initial thick and thin filaments and sarcomeres are much shorter than adult length. Sarcomere length increases smoothly and coordinately from approximately 1.7 to approximately 3.2 microns, reflecting increase in filament lengths and indicating that myosin and actin molecules must be incorporated into filaments after sarcomere formation. Myofilaments are not seen scattered in the cytoplasm at any time, nor do we detect filaments that could be in the process of being "trolleyed" along myofibrils into positions of lateral register. Myofibril diameter increases uniformly from approximately 4-thick filaments to approximately 36-thick filaments across, by peripheral addition of myofilaments. At each successive stage, all sarcomeres in a fiber attained similar length and diameter. Initial thick filaments are solid but within several hours these and all subsequently assembled thick filaments appear hollow. Initial Z-bodies do not show any internal lattice and are more irregularly shaped than adult Z-discs.
Animals↗
A new MR-compatible loading device to study in vivo muscle damage development in rats due to compressive loading.
To study the aetiology of pressure ulcers an MR-compatible loading device was developed. Magnetic resonance imaging provides the possibility of non-invasive evaluation of muscle tissue after compressive loading. Pressure was applied to the tibialis anterior region of rats by means of an indenter. The developed MR-compatible loading device allowed high quality consecutive MR measurements for up to 6h. Tissue was evaluated both during and after loading. Two loading protocols were used; a large indentation of 4.5mm (mean pressure 150 kPa) was applied for 2h and a small indentation of 2.9 mm (mean pressure 50 kPa) was applied for 4h. T2-weighted MR images after the large indentation showed an immediate increase in signal intensity, associated with damage, following load removal. After 20 h the signal intensity remained higher in the affected regions. Afterwards the tissue was perfusion fixated for histological examination. Histological evaluation revealed an inflammatory response and severe muscle necrosis. No signal increase was observed after small indentation. With this new set-up, the different factors that may play a role in the onset of muscle damage can be studied, what we believe will lead to a better understanding of the contributing factors to pressure ulcer development.
Animals↗
Osteopontin expression in coculture of differentiating rat fetal skeletal fibroblasts and myoblasts.
Skeletal fibroblasts in vitro can acquire myofibroblast phenotypes by the development of biochemical and morphological features, mainly the expression of alpha-smooth-muscle actin (alpha-SMA). Myogenic differentiation is a central event in skeletal muscle development, and has commonly been studied in vitro in the context of skeletal muscle development and regeneration. Controlling this process is a complex set of interactions between myoblasts and the extracellular matrix. Osteopontin (OPN) is an acidic, phosphorylated matrix protein that contains an Arg-Gly-Asp (RGD) cell attachment sequence and has been identified as an adhesive and migratory substrate for several cell types. The aim of this study was to investigate osteopontin expression during the differentiation of skeletal fibroblasts into myofibroblasts and during myogenesis in a coculture model. Fibroblasts and myoblasts were obtained from skeletal muscle of 18-d-old Wistar strain rat fetuses by enzymatic dissociation. At 1 and 9 d, cocultures were immunolabeled, and the cells were also separately subjected to Western blotting to analyze OPN expression. Our data using confocal microscopy showed that myoblasts displayed a strong staining for OPN and that this labeling was maintained after myotube differentiation. Conversely, during fibroblast differentiation into myofibroblasts, we observed a significant increase in OPN expression. The results obtained by immunolabeling were confirmed by Western blotting. We suggest that OPN is important mainly during early stages of myogenesis, facilitating myoblast fusion and differentiation, and that the increased expression of OPN in myofibroblasts might be related to its effects as a key cytokine regulating tissue repair and inflammation.
Animals↗
Identification of two variants of troponin T in the developing chicken heart using a monoclonal antibody.
Troponin T (TNT) expressed in the developing chicken cardiac muscle was examined by immunoblotting combined with two-dimensional electrophoresis (2-D PAGE) and peptide mapping. When the whole lysate of the neonatal heart was examined by 2-D PAGE, two TNT variants were detected on the gel by monoclonal antibody to TNT. Expression of the two variants was developmentally regulated: one isoform (type I) was expressed from embryonic through neonatal stages, and the other (type II) from the late embryonic stage through adulthood during cardiac muscle development. The type-I isoform, but not type-II isoform, was also expressed transiently in chicken skeletal muscle at embryonic stages. As judged from the peptide maps, the two isoforms differed in the N-terminal region but not in the C-terminal region.
Aging↗
Ultrastructure of the tracheal muscle in developing, adult and ageing guinea-pigs.
The musculature of the trachea of adult guinea-pigs is ultrastructurally similar to other visceral muscles. However, tracheal muscle cells have irregular outlines, large accumulations of glycogen, a small number of gap junctions, and many small elastic fibres and collagen fibrils (50 nm in diameter). Fibroblasts, mast cells, Schwann cells and axons are found within the muscle, but no interstitial cells. Capillaries run in the connective tissue septa. The tracheal muscle is well differentiated at the end of the fetal life. At this time, muscle cells have an appearance similar to that of a mature muscle. However, the cells are smaller, especially in length, and their orientation is less regular. There are no undifferentiated cells; a few muscle cells are seen in mitosis. There is a limited amount of stroma, mainly small collagen fibrils not exceeding 30 nm in diameter. Within the muscle there are many nerves, but no fibroblasts or mast cells. Many structural contacts link together the muscle cells, but there are no gap junctions. Gap junctions develop in the first few days after birth and are distinct in 5-day-old animals. In ageing guinea-pigs (30-36 months old) the muscle cells are slightly larger than in the young adult. They display deep invaginations of the cell membrane and a very irregular profile. There is an increase in the number of glycogen granule clusters, and the basal lamina is particularly prominent. The amount of stroma has increased, and is made of large elastic fibres and collagen fibrils up to 105 nm in diameter.
Aging↗
Effect of hypothyroidism on the expression of cytochrome c and cytochrome c oxidase in heart and muscle during development.
The effect of thyroid hormone on the expression of mitochondrial proteins was evaluated during development by measuring cytochrome c oxidase (CYTOX) activity and cytochrome c protein and mRNA levels in heart and skeletal muscle of control and hypothyroid rats. Animals were killed at the late fetal, early, and late postnatal stages up to 56 days of age. In heart, CYTOX activity increased 2.3-fold above the fetal level throughout development, most of which occurred prior to 2 days of age. No increase was observed in muscle. CYTOX activity was reduced in hypothyroid animals throughout development in heart compared to controls (by 50% at 56 days), but in muscle no effect of hypothyroidism was observed. In muscle and heart 4- and 1.5-fold increases in cytochrome c above the fetal level were evident by 1 day of age, with further increases to 8.5- and 2.7-fold by 56 days, respectively. The increase in cytochrome c differed from the increase in CYTOX, indicating changes in mitochondrial composition. Hypothyroidism reduced cytochrome c in muscle by 30-35% at 56 days, but had no effect in heart, indicating a muscle type-specific effect of thyroid hormone on cytochrome c protein expression. Cytochrome c mRNA increased rapidly to 4-5 fold above the fetal level in both heart and muscle by 6 h post-partum. Between 7 and 56 days of age, further increases to 6- and 25-fold were observed in muscle and heart, respectively. In muscle, the 6-fold developmental increase in mRNA paralleled that of the protein, suggesting transcriptional regulation.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Time course of ion channel development in Xenopus muscle induced in vitro by activin.
During the process of mesoderm specification in Xenopus embryos, cells of the equatorial region are induced to form mesoderm in response to signals from the underlying endodermal cells. One mesodermal cell type resulting from this in vivo induction is skeletal muscle, which has a very specific and tightly regulated course of electrical and morphological development. Previously, electrical development could be analyzed only after neurulation, once myocytes could be morphologically identified. In vitro, activin triggers a cascade of events leading to the development of specific mesodermal tissues, including skeletal muscle; however, the precise role of activin in vivo is less clear. Much is now known about the mechanism and control of activin action, but very little is known about the subsequent time course of differentiation of activin-induced muscle. Such muscle is routinely identified by the presence of a small number of specific markers which, although they accurately confirm the presence of muscle, give little indication of the time course or quantitative aspects of muscle development. One of the most important functional aspects of muscle development is the acquisition of the complex electrical properties which allow it to function normally. Here we assess the ability of activin to drive in vitro the normal highly regulated sequence of electrical development in skeletal muscle. We find that in most, but not all, respects the normal time course of development of voltage-gated ion currents is well reproduced in activin-induced muscle. This characterization strengthens the case for activin as an agent capable of inducing the detailed developmental program of muscle and now allows for analysis of the regulation of electrical development prior to neurulation.
Activins↗
Role of exogenous and endogenous trophic factors in the regulation of extraocular muscle strength during development.
PURPOSE: Weak eye muscles can cause ophthalmic disorders, and in particular, strabismus. Exogenous trophic factors such as cardiotrophin (CT)-1 and insulin-like growth factor (IGF) have been shown to increase the contractile force of adult heart and skeletal muscles, respectively. In the current study, the effects of endogenous and exogenous trophic factors on extraocular muscle strength and mass were examined in the developing chicken. METHODS: Superior rectus and superior oblique muscles of hatchling chicks were treated in vivo either to increase levels of trophic factors CT-1, IGF-I, glial cell line-derived neurotrophic factor (GDNF), or brain-derived neurotrophic factor (BDNF), or to decrease their levels with neutralizing antibodies and binding proteins. Forty-eight hours after factors were injected into the orbit, the contractile force of dissected muscles was measured in vitro and the morphology of muscle fibers was compared between control and treated muscles. RESULTS: Treatment with CT-1 or IGF-I significantly increased the mean single-twitch force generation and these trophic factors increased muscle fiber diameters when compared to control muscles. A cocktail of antibodies and binding proteins, directed against endogenous IGF-I, GDNF, and CT-1, significantly decreased mean single-twitch force. This cocktail slightly, but significantly, reduced muscle fiber diameters within treated extraocular muscles. CONCLUSIONS: Endogenous trophic factors regulate and/or maintain extraocular muscle force through a rapid mechanism that appears to involve changes in muscle mass and specifically enlargement of muscle fiber diameters. CT-1 and IGF-I may be considered promising candidate trophic factors for therapeutic strengthening of eye muscles in the developing extraocular muscle system.
Animals↗
The level of natural antioxidant glutathione and histidine-containing dipeptides in skeletal muscles of developing chick embryos.
1. The levels of glutathione and histidine-containing dipeptides in skeletal muscles change in different ways during ontogenesis. 2. The glutathione content in skeletal muscles increases between the 9th and 18th days of embryongenesis--from 0.5 to 2.0 mumol/g of tissue wet wt and then drops to zero in 3-week-old chickens. 3. The level of histidine-containing dipeptides increases throughout the observation period beginning with their appearance on the 14th day in leg muscles and on the 15th day in breast muscles of chicken embryos up to the 21st postnatal day. 4. There is a negative correlation between the antioxidative systems of glutathione and histidine-containing dipeptides in muscle tissue, i.e. dipeptide-rich tissues contain little or no glutathione and vice versa.
Animals↗
Permissive roles of phosphatidyl inositol 3-kinase and Akt in skeletal myocyte maturation.
Skeletal muscle differentiation, maturation, and regeneration are regulated by interactions between signaling pathways activated by hormones and growth factors, and intrinsic genetic programs controlled by myogenic transcription factors, including members of the MyoD and myocyte enhancer factor 2 (MEF2) families. Insulin-like growth factors (IGFs) play key roles in muscle development in the embryo, and in the maintenance and hypertrophy of mature muscle in the adult, but the precise signaling pathways responsible for these effects remain incompletely defined. To study mechanisms of IGF action in muscle, we have developed a mouse myoblast cell line termed C2BP5 that is dependent on activation of the IGF-I receptor and the phosphatidyl inositol 3-kinase (PI3-kinase)-Akt pathway for initiation of differentiation. Here, we show that differentiation of C2BP5 myoblasts could be induced in the absence of IGF action by recombinant adenoviruses expressing MyoD or myogenin, but it was reversibly impaired by the PI3-kinase inhibitor LY294002. Similar results were observed using a dominant-negative version of Akt, a key downstream component of PI3-kinase signaling, and also were seen in C3H 10T1/2 fibroblasts. Inhibition of PI3-kinase did not prevent accumulation of muscle differentiation-specific proteins (myogenin, troponin T, or myosin heavy chain), did not block transcriptional activation of E-box containing muscle reporter genes by MyoD or myogenin, and did not inhibit the expression or function of endogenous MEF2C or MEF2D. An adenovirus encoding active Akt could partially restore terminal differentiation of MyoD-expressing and LY294002-treated myoblasts, but the resultant myofibers contained fewer nuclei and were smaller and thinner than normal, indicating that another PI3-kinase-stimulated pathway in addition to Akt is required for full myocyte maturation. Our results support the idea that an IGF-regulated PI3-kinase pathway functions downstream of or in parallel with MyoD, myogenin, and MEF2 in muscle development to govern the late steps of differentiation that lead to multinucleated myotubes.
Animals↗
Expression of aldolase A steady-state mRNA is delayed relative to other muscle-specific genes during differentiation of chicken myoblasts.
Expression of several muscle-specific genes was monitored during chicken muscle development and myoblast differentiation in primary cultures. The individual patterns of expression for many muscle-specific genes are well documented in ovo and in other model systems of muscle development. However, comparison of aldolase A to other muscle-specific genes in one system has not been reported. Both sarcomeric and cytosolic genes important for the adult muscle fiber were examined in order to elucidate their timing of expression and its relationship to cell fusion. Steady-state mRNA expression was measured using RNase protection assays with cRNA probes generated from cDNA clones for muscle creatine kinase, fast skeletal troponin-T, embryonic myosin heavy chain, and aldolase A. Nonmuscle genes expressed largely in the embryo, aldolase C and beta-actin, were used as controls. The expression of all six genes revealed differences in temporal expression patterns between limb and axial muscle. The temporal expression patterns of all six genes were also monitored in primary myoblast cultures relative to myoblast fusion. In both axial and limb myoblast cultures most of the muscle-specific genes were expressed prior to fusion. During the differentiation of myoblasts to myotubes there was a biphasic pattern in the expression of the muscle-specific genes. The appearance of measurable mRNA was detected by 16 hr in culture, prior to appreciable fusion of the cells. During further differentiation the expression increased gradually and then more rapidly at 96 hr, once fusion was complete. Meanwhile, the nonmuscle embryonic gene expression declined only slightly. For one gene, aldolase A, expression was delayed relative to the other muscle-specific genes, both in the appearance of measurable mRNA and in the later rapid increase in mRNA.
Animals↗