Mechanisms of muscle growth and repair. Loss of muscle protein stores can result from three responses: impaired growth of new muscle fibres, suppression of protein. Altmetric: 42; Views: 5,708; More detail. Cryotherapy Reduces Inflammatory Response Without Altering Muscle Regeneration Process and Extracellular. Myostatin Mutation Associated with Gross Muscle Hypertrophy in a Child. Markus Schuelke, M.D., Kathryn R. Wagner, M.D., Ph.D., Leslie. Peripheral muscle wasting is a common finding in advanced chronic obstructive pulmonary disease (COPD) and several other chronic diseases. Allele Name: X linked muscular dystrophy: Allele Type: Spontaneous: Allele Synonym(s) mdx; pke; pyruvate kinase expression: Gene Symbol and Name: Dmd, dystrophin. Local Expression Of Igf-1 Accelerates Muscle Regeneration By PatLocal Expression Of Igf-1 Accelerates Muscle Regeneration By BarkerMost pathogenic bacteria require iron to survive, and in order to acquire iron in the relatively iron- scarce oral cavity A. The genes encoding these siderophores and transporters are thought to be regulated by the amount of iron in the growth medium and by the metal- dependent repressor, Amd. R, which we showed previously binds to the promoter of proposed iron- regulated genes. Objective The purpose of this study was to characterize siderophore and associated iron transport systems in A. Design We examined gene expression of the putative iron transport genes fet. A and sid. D in response to low- and high- iron environments. One of these genes, sid. Mechanisms of Disease. Epstein, M.D., Editor. Role of Transforming Growth Factor . D, encoding a putative Fe ABC transporter protein, was insertionally inactivated and was examined for causing growth defects. To gain a further understanding of the role of iron metabolism in oral diseases, clinical isolates of Actinomyces spp. One of these genes (sid. D) was mutated, and the sid. D: :Km strain exhibited a 5. This growth defect was restored when the sid. D gene was provided in a complemented strain. We were able to isolate the Amd. R- encoding gene in seven clinical isolates of Actinomyces. When these protein sequences were aligned to the laboratory strain, there was a high degree of sequence similarity. Conclusions The growth of the sid. D: :Km mutant in iron- replete medium mirrored the growth of the wild- type strain grown in iron. Skeletal muscle sarcolemma in malignant hyperthermia: evidence for a defect in calcium regulation. Pub. Med. Mickelson, J R; Ross, J A; Hyslop, R J; Gallant, E M; Louis, C F1. Sarcolemmal properties implicated in the skeletal muscle disorder, malignant hyperthermia (MH), were examined using sarcolemma- membrane vesicles isolated from normal and MH- susceptible (MHS) porcine skeletal muscle. MHS and normal sarcolemma did not differ in the distribution of the major proteins, cholesterol or phospholipid content, vesicle size and sidedness, (Na+ + K+)- ATPase activity, ouabain binding, or adenylate cyclase activity (total and isoproterenol sensitivity). The regulation of the initial rates of MHS and normal sarcolemmal ATP- dependent calcium transport (calcium uptake after 1 min) by Ca. K1/2 = 0. 6. 4- 0. M), calmodulin, and c. AMP- dependent protein kinase were similar. However, when sarcolemmal calcium content was measured at either 2 or 2. MHS and normal sarcolemmal calcium uptake became apparent, with MHS sarcolemma accumulating approximately 2. Calcium transport by MHS and normal sarcolemma, at 2 or 2. C1/2 = 1. 50 n. M), and was stimulated to a similar extent by c. AMP- dependent protein kinase or calmodulin. Halothane inhibited MHS and normal sarcolemmal active calcium uptake in a similar fashion (half- maximal inhibition at 1. M halothane), while dantrolene (3. M) and nitrendipine (1 micro. M) had little effect on either MHS or normal sarcolemmal calcium transport. After 2. 0 min of ATP- supported calcium uptake, 2 m. M EGTA plus 1. 0 micro. M sodium orthovanadate were added to initiate sarcolemmal calcium efflux. Following an initial rapid phase of calcium release, an extended slow phase of calcium efflux (k = 0. MHS and normal sarcolemma vesicles. We conclude that although a number of sarcolemmal properties, including passive calcium permeability, are normal in MH, a small but significant defect in MHS sarcolemmal ATP- dependent calcium transport may. Cryptorchidism in the Orl Rat Is Associated with Muscle Patterning Defects in the Fetal Gubernaculum and Altered Hormonal Signaling. Pub. Med Central. Barthold, Julia S.; Robbins, Alan; Wang, Yanping; Pugarelli, Joan; Mateson, Abigail; Anand- Ivell, Ravinder; Ivell, Richard; Mc. Cahan, Suzanne M.; Akins, Robert E. ABSTRACT Cryptorchidism, or undescended testis, is a common male genital anomaly of unclear etiology. Hormonal stimulation of the developing fetal gubernaculum by testicular androgens and insulin- like 3 (INSL3) is required for testicular descent. In studies of the orl fetal rat, one of several reported strains with inherited cryptorchidism, we studied hormone levels, gene expression in intact and hormone- stimulated gubernaculum, and imaging of the developing cremaster muscle facilitated by a tissue clearing protocol to further characterize development of the orl gubernaculum. Abnormal localization of the inverted gubernaculum was visible soon after birth. In the orl fetus, testicular testosterone, gubernacular androgen- responsive transcript levels, and muscle- specific gene expression were reduced. However, the in vitro transcriptional response of the orl gubernaculum to androgen was largely comparable to wild type (wt). In contrast, increases in serum INSL3, gubernacular INSL3- responsive transcript levels, expression of the INSL3 receptor, Rxfp. INSL3 in vitro all suggest enhanced activation of INSL3/RXFP2 signaling in the orl rat. However, DNA sequence analysis did not identify functional variants in orl Insl. Finally, combined analysis of the present and previous studies of the orl transcriptome confirmed altered expression of muscle and cellular motility genes, and whole mount imaging revealed aberrant muscle pattern formation in the orl fetal gubernaculum. The nature and prevalence of developmental muscledefects in the orl gubernaculum are consistent with the cryptorchid phenotype in this strain. These data suggest impaired androgen and enhanced INSL3 signaling in the orl fetus accompanied by defective cremaster muscle development. PMID: 2. 49. 66. 39. Defective collagen VI . Here we report that the . By contrast, the collagen VI . In vitro treatment with TGF- . PMID: 2. 49. 07. 56. Defective collagen VI . Here we report that the . By contrast, the collagen VI . In vitro treatment with TGF- . PMID: 2. 49. 07. 56. Defective regulation of energy metabolism in mdx- mouse skeletal muscles. Pub. Med. Even, P C; Decrouy, A; Chinet, A1. Our previous finding of a reduced energy metabolism in slow- and fast- twitch skeletal muscle fibres from the murine model of Duchenne muscular dystrophy (the mdx mouse) led us to examine the importance of intracellular glucose availability for a normal energy turnover. To this end, basal and KCl- stimulated (2. M total extracellular K+) rates of glucose uptake (GUP) and heat production were measured in isolated, glucose- incubated (5 m. M) soleus and extensor digitorum longus muscles from mdx and control C5. B1/1. 0 mice, in the presence and in the absence of insulin (1. M). Under all conditions and for both muscle types, glucose uptake values for mdx and control muscles were similar although heat production was lower in mdx muscles. The marked stimulation of GUP by insulin in both mdx and control muscles had only minor effects on heat production. In contrast, glucose deprivation or inhibition of glycolysis with 2- deoxy- D- glucose (5 m. M) significantly decreased heat production in control muscles only, which attenuated, although did not suppress, the difference in basal heat production between mdx and control muscles. Stimulation of heat production by a short- chain fatty acid salt (octanoate, 2 m. M) was significantly less marked in mdx than in control muscles. Increased cytoplasmic synthesis of Co. A by addition of 5 m. M pantothenate (vitamin B5) increased the thermogenic response to glucose more in mdx than in control muscles. We conclude that the low energy turnover in mdx- mouse muscle fibres is not due to a decrease of intracellular glucose availability, but rather to a decreased oxidative utilization of glucose and free fatty acids. We suggest that some enzyme complex of the tricarboxylic acid cycle or inefficiency of Co. A transport in the mitochondria could be involved. PMID: 7. 99. 90. 03. Defective Natriuretic Peptide Receptor Signaling in Skeletal Muscle Links Obesity to Type 2 Diabetes. Pub. Med. Cou. Since skeletal muscle was recently shown as a key target tissue of NP, we aimed to investigate muscle NP receptor (NPR) expression in the context of obesity and T2. D. Muscle NPRA correlated positively with whole- body insulin sensitivity in humans and was strikingly downregulated in obese subjects and recovered in response to diet- induced weight loss. In addition, muscle NP clearance receptor (NPRC) increased in individuals with impaired glucose tolerance and T2. D. Similar results were found in obese diabetic mice. Although no acute effect of brain NP (BNP) on insulin sensitivity was observed in lean mice, chronic BNP infusion improved blood glucose control and insulin sensitivity in skeletal muscle of obese and diabetic mice. This occurred in parallel with a reduced lipotoxic pressure in skeletal muscle due to an upregulation of lipid oxidative capacity. In addition, chronic NP treatment in human primary myotubes increased lipid oxidation in a PGC1. Collectively, our data show that activation of NPRA signaling in skeletal muscle is important for the maintenance of long- term insulin sensitivity and has the potential to treat obesity- related metabolic disorders. PMID: 2. 62. 53. 61. Muscle inactivation of m. TOR causes metabolic and dystrophin defects leading to severe myopathy. Pub. Med Central. Risson, Val. Raptor is required for oxidative muscle integrity, whereas rictor is dispensable. In this study, we show that muscle- specific inactivation of m. TOR leads to severe myopathy, resulting in premature death. In addition, m. TOR- deficient muscles exhibit increased basal glucose uptake, whereas whole body glucose homeostasis is essentially maintained. Importantly, loss of m. TOR exacerbates the myopathic features in both slow oxidative and fast glycolytic muscles. Moreover, m. TOR but not raptor and rictor deficiency leads to reduced muscle dystrophin content. We provide evidence that m. TOR controls dystrophin transcription in a cell- autonomous, rapamycin- resistant, and kinase- independent manner. Collectively, our results demonstrate that m. TOR acts mainly via m. TORC1, whereas regulation of dystrophin is raptor and rictor independent. PMID: 2. 00. 08. 56.
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