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PubMed2005

Smooth muscle in the female pelvic peritoneum: a clinicopathological analysis of 31 women.

AIM: To study the presence and morphological features of smooth muscle in the subcoelomic mesenchyme with the aim of establishing both a normal range for the female pelvis, and its possible relationship to endometriosis, diffuse peritoneal leiomyomatosis (LPD) and other forms of 'müllerianosis'. METHODS: Seventy laparoscopically obtained pelvic peritoneal biopsies accessioned over a 16-month period were examined from 31 women clinically suspected of endometriosis. These biopsies were selected for the presence of assessable, appropriately oriented peritoneum, sufficiently distant from focal endometriosis to allow a presumption of 'normality'. The histological features and morphometric measurements of smooth muscle in these biopsies were documented. Pathological changes, where present, were recorded. RESULTS: Focal endometriosis was identified in 28 (40%) of the biopsies, nine (12.9%) displayed other manifestations of 'müllerianosis', 11 (15.7%) showed focal chronic inflammation or fibrosis only, and 22 (31.4%) displayed no specific pathological changes. Of 70 biopsies, 52 contained smooth muscle within the subcoelomic mesenchyme, directly below the peritoneal mesothelium. Biopsies in which smooth muscle was identified were predominantly from the region of the uterosacral ligaments (16/18) and pelvic side wall (22/25). The biopsies without a smooth muscle layer were predominantly from the pararectal area (7/8) or the rectal serosa (2/4). Where present, smooth muscle varied in prominence, depth, thickness of the layer and organisation of muscle bundles. Patterns ranged from thin, widely spaced and wispy fibres to a more or less continuous band of either horizontally and/or vertically organised fibres. Both focal and diffuse arrangements were evident. 'Neovascularisation' was observed laparoscopically in some areas that corresponded with prominent smooth muscle development. CONCLUSIONS: Smooth muscle occurs sufficiently frequently immediately beneath the peritoneum of the female pelvis, and with a sufficiently predictable anatomical distribution, to be regarded as a normal component of the microanatomy of this tissue in the patients studied.

Adult↗
PubMed1996

Elevated catalase activity in red and white muscles of MyoD gene-inactivated mice.

MyoD is a myogenic transcription factor responsible for skeletal muscle differentiation during development. Muscle antioxidant enzyme status was determined in transgenic MyoD deactivated mice. While catalase activity was significantly (P < 0.05) elevated in soleus and extensor digitorum longus muscles from MyoD deactivated mice, superoxide dismutase and glutathione peroxidase activities were not. While this may imply a greater propensity for inherent oxidative stress, soleus glutathione status was similar between MyoD deactivated mouse and control soleus muscles. Catalase activity is localized primarily in peroxisomes. Therefore elevated catalase activity may also indicate the presence of factors associated with peroxisome proliferation in muscles from MyoD gene-inactivated mice.

Animals↗
PubMed1993

Human nicotinic acetylcholine receptor alpha-subunit isoforms: origins and expression.

A majority of the autoantibodies in the disease myasthenia gravis (MG) are directed against the alpha-subunit of the muscle nicotinic acetylcholine receptor (AChR). Unlike AChR alpha-subunits previously characterised from other species, the human alpha-subunit exists as two isoforms. The isoforms are generated by alternate splicing of an additional exon located between exons P3 and P4, termed P3A. The 25 amino acids encoded by the P3A exon are incorporated into the extracellular region of the alpha-subunit, and so may be relevant to the pathogenesis of MG. Genomic sequences from rhesus monkey, and from dog and cat, which are susceptible to MG, were characterised between AChR alpha-subunit exons P3 and P4. Although regions homologous to the P3A exon were identified for each of these species, analysis by RT-PCR showed that they are not expressed. At variance with a previous report, constitutive expression of mRNA encoding the human P3A+ alpha-subunit isoform was not detected in heart, kidney, liver, lung or brain. Differential expression of the two alpha-subunit isoforms was not seen during fetal muscle development or in muscle from MG patients. In all cases where mRNAs encoding the two alpha-subunit isoforms have been detected, they are present at an approximate 1:1 ratio.

Alternative Splicing↗
PubMed1989

An actin-depolymerizing protein in embryonic chicken skeletal muscle: purification and characterization.

In embryonic skeletal muscle, a large amount of non-polymerized actin exists in the cytoplasm (Shimizu and Obinata [1986] J. Biochem. 99, 751-759). A 19-kDa protein (called 19K protein) which binds to G-actin was purified by sequential chromatography on DNase I-agarose, hydroxylapatite, SP-Sephadex, and Sephadex G-75, from the sarcoplasmic fraction of embryonic chicken skeletal muscle. This protein decreased the extent of actin polymerization at a steady state and increased the monomeric actin in a concentration-dependent fashion; it also caused quick depolymerization of F-actin, as determined by spectrophotometry at 237 nm, viscometry, DNase I inhibition assay, and electron microscopy. The molar ratio of 19K protein and actin interacting with each other was estimated to be 1:1. From these results, 19K protein was regarded as being actin depolymerizing protein. The amount of 19K protein in muscle decreased during development. The inhibitory action of 19K protein was removed by myosin or heavy meromyosin, and actin filaments were formed on the surface of myosin filaments when myosin filaments were added to a mixture of actin and 19K protein in a physiological salt solution. We propose that actin assembly is dually controlled in the developing muscle by the inhibitor(s) and an accelerator (myosin); this mechanism may enable the ordered assembly of actin and myosin in the early phase of myofibrillogenesis.

Actin Cytoskeleton↗
PubMed1978

Experimental transformation of muscle fiber properties in lobster.

Like the chelipeds, the claw closer muscles of the adult lobster are asymmetric (dipmorphic). In the crusher claw the closer muscle is composed entirely of slow fibers, and in the cutter claw it has 65 to 75 percent fast fibers and 25 to 35 percent slow fibers. While claw placement in the adult is essentially random, it can be demonstrated in two ways that the muscle fiber properties are not genetically fixed: (i) if one claw is removed in the fourth and early fifth stages, the remaining closer muscle develops all slow muscle fibers, and (ii) if the animals are raised in smooth-bottomed containers, both claws can become cutter types, having closer muscles with more than 50 percent fast fibers. Thus, as in vertebrate skeletal muscle, the properties of lobster closer muscle fibers can be transformed by various experimental manipulations.

Animals↗
PubMed2000

Involvement of Ras and Ral in chemotactic migration of skeletal myoblasts.

In skeletal myoblasts, Ras has been considered to be a strong inhibitor of myogenesis. Here, we demonstrate that Ras is involved also in the chemotactic response of skeletal myoblasts. Expression of a dominant-negative mutant of Ras inhibited chemotaxis of C2C12 myoblasts in response to basic fibroblast growth factor (bFGF), hepatocyte growth factor (HGF), and insulin-like growth factor 1 (IGF-1), key regulators of limb muscle development and skeletal muscle regeneration. A dominant-negative Ral also decreased chemotactic migration by these growth factors, while inhibitors for phosphatidylinositol 3-kinase and mitogen-activated protein kinase kinase (MEK) showed no effect. Activation of the Ras-Ral pathway by expression of an activated mutant of either Ras, the guanine-nucleotide dissociation stimulator for Ral, or Ral resulted in increased motility of myoblasts. The ability of Ral to stimulate motility was reduced by introduction of a mutation which prevents binding to Ral-binding protein 1 or phospholipase D. These results suggest that the Ras-Ral pathway is essential for the migration of myoblasts. Furthermore, we found that Ras and Ral are activated in C2C12 cells by bFGF, HGF and IGF-1 and that the Ral activation is regulated by the Ras- and the intracellular Ca(2+)-mediated pathways. Taken together, our data indicate that Ras and Ral regulate the chemotactic migration of skeletal muscle progenitors.

Animals↗
PubMed1987

Intramuscular pressure and muscle blood flow during exercise in chronic compartment syndrome.

In nine patients with chronic compartment syndrome, the intramuscular pressure and muscle blood flow during constant dynamic exercise was studied by the microcapillary infusion method and by the 133-xenon clearance technique. Although muscle blood flow was normal at the start of exercise, pain and impaired muscle function eventually developed; muscle blood flow decreased while muscle relaxation pressure increased. The changes of muscle blood flow could not be correlated with any change of mean muscle pressure during exercise. Eight months after fasciotomy the exercise test was repeated. Patients experienced no symptoms and the muscle relaxation pressure and blood flow during exercise were normal. It is suggested that chronic compartment syndrome is due to increased muscle relaxation pressure during exercise which causes decreased muscle blood flow, leading to ischaemic pain and impaired muscle function.

Adolescent↗
PubMed1996

Identification and characterization of a 47 base pair activity-dependent enhancer of the rat nicotinic acetylcholine receptor delta-subunit promoter.

Nicotinic acetylcholine receptor (nAChR) genes are regulated by muscle electrical activity. E-box sequences found in their promoters are necessary for this regulation. However, many muscle genes contain E-boxes, yet are not regulated by muscle depolarization. This suggests that other elements are necessary, perhaps working in conjunction with E-boxes, to confer depolarization-dependent control onto promoter activity. We have used direct DNA injection into muscle as an in vivo assay to identify and characterize these additional elements. Mutagenesis and expression assays identified multiple elements within the first 81 base pairs (bp) of the nAChR delta-subunit promoter that contribute to its regulation by muscle electrical activity. Within this 81 bp sequence, two regions of DNA were identified that were capable of conferring activity-dependent regulation onto a heterologous promoter. The stronger of these two putative enhancers was characterized further. It is a 47 bp sequence that contains an E-box along with sequences similar to the SV40 core enhancer and an SP1 site. Site-directed mutagenesis identified residues within each of these sequences that were necessary for enhancer activity. Furthermore, methylation interference DNA footprinting assays showed increased nuclear protein binding to sequences within both these enhancers after muscle denervation, and this pattern of binding was very similar to that observed with nuclear protein isolated from myotube extracts. These latter results suggest that similar mechanisms may mediate increased nAChR expression during muscle development and after muscle denervation.

Animals↗
PubMed1996

Autonomous and nonautonomous Notch functions for embryonic muscle and epidermis development in Drosophila.

The Notch (N) gene encodes a cell signaling protein that mediates neuronal and epidermal determination in Drosophila embryos. N also regulates several aspects of myogenic development; embryos lacking N function have too many muscle founder cells and fail to properly differentiate somatic muscle. To identify cell-autonomous requirements for Notch function during muscle development, we expressed a Notch minigene in the mesoderm, but not in the ectoderm, of amorphic N-embryos. In these embryos, muscle founder hypertrophy is rescued, indicating that Notch is autonomously required by mesoderm cells to regulate the proper number of muscle founders. However, somatic muscle differentiation is only partially normalized, suggesting that Notch is also required in the ectoderm for proper muscle development. Additionally, mesodermal expression of Notch partially rescues epidermal development in overlying neurogenic ectoderm. This is unexpected, since previous studies suggest that Notch is autonomously required by proneural ectoderm cells for epidermal development. Mesodermal expression of a truncated Notch protein lacking the extracellular domain does not rescue ventral epidermis, suggesting that the extra-cellular domain of Notch can non-autonomously rescue epidermal development across germ layers.

Animals↗
PubMed1989

Inhibition of myogenic differentiation by the H-ras oncogene is associated with the down regulation of the MyoD1 gene.

Skeletal muscle development is regulated by a complex series of genetic and environmental cues that control the establishment of the myogenic lineage and the differentiation of determined myoblasts. Numerous agents, including growth factors and oncogene products, have been shown to inhibit skeletal muscle development, possibly by affecting the pattern of signal transduction that is required for myogenesis. Among the eukaryotic G proteins that have been implicated as mediators of signal transduction are the protein products of the mammalian ras genes (p21s). In this study, we demonstrate that expression of a transfected, oncogenic, human H-ras gene in C3H10T1/2-derived myoblasts has dramatic, yet varied, effects on skeletal myogenesis. While some H-ras transformed myoblast clones are differentiation-defective, other clones are inhibited from morphologically differentiating but retain a limited ability to biochemically differentiate. The H-ras induced inhibition of differentiation usually is associated with a decreased expression of the myogenic determination gene, MyoD1. Introduction of a MyoD1 cDNA expression vector into differentiation-defective H-ras expressing myoblasts partially restores the myogenic potential in these cells. Our results suggest that activated H-ras p21 inhibits the terminal differentiation of myoblasts by producing a general reduction in the differentiation competence of cells which, in the most extreme case, is a consequence of the down-regulation of the MyoD1 determination gene.

Animals↗
PubMed1985

Characterization of cDNA and genomic sequences corresponding to an embryonic myosin heavy chain.

We report here the isolation and characterization of cDNA and genomic sequences corresponding to a rat embryonic myosin heavy chain (MHC) protein. This gene, which is present as a single copy in the rat genome, comprises about 25 kilobase pairs of DNA and contains approximately 80% intronic sequences. The embryonic MHC gene belongs to a highly conserved multigene family, and exhibits a high degree of nucleotide and amino acid sequence conservation with other sarcomeric MHC genes from nematode to man. S1 nuclease mapping experiments using cDNA and genomic probes show that this MHC gene is transiently expressed during skeletal muscle development. Its mRNA is detected in fetal skeletal muscle during early development and persists up to 2 weeks after birth with the overlapping expression of neonatal and adult skeletal MHC mRNAs. However, this MHC is not expressed in the adult skeletal muscle with the exception of extraocular muscle fibers. The transient expression during muscle development of the isoform produced by this gene and its sequential replacement by other MHCs raises interesting questions about the mechanism controlling MHC isozyme transitions and the physiological significance of the individual MHCs in muscle fibers.

Animals↗
PubMedDate not supplied

[Structure and functions of muscle allotransplants developing in adrenals and the alloplasty area after long-term exposure].

The cross allotransplantation of right gastrocnemius muscles was carried out between intact rats and rats in which adrenals and right shins were subjected to low-energy He-Ne laser radiation (10 procedures for 2 weeks, the exposure duration 5 min; total dose for each rat 15-18 J/cm2). By conditions of experiment, the rats in each series were both donors and recipients, and hence the heterogeneity of rats in each series was the same. It was shown that the laser radiation in the dose studied and the regimes of exposure of rat adrenals and shin (area of the planned allotransplantation) influenced the muscle alloplasty. In rats with irradiated adrenals and shin, the disintegration and resorption of muscle allografts occurred more actively. In intact rats, muscle allografts were more viable. The allogenic muscle tissue and a weak contractile reaction of allografts were revealed in most of them. The allografts showed a moderate lymphocytic infiltration. The data obtained indirectly evidence that the transplant immune reaction increased in rats with irradiated adrenals and shin. In intact rats, the transplant immune reaction to irradiated m.gastrocnemius from irradiated shin decreased.

Adrenal Glands↗
PubMed2004

Effects of hypophysectomy and recombinant human growth hormone on material and geometric properties and the pre- and post-yield behavior of femurs in young rats.

To study the musculoskeletal effects of hypophysectomy (Hx) and a partial replacement treatment with recombinant human growth hormone (rhGH) in rats, we determined the stiffness (elastic modulus, E) and volumetric BMD (vBMD) of cortical bone; the periosteal and endosteal perimeters, area and bending moment of inertia (xCSMI) of the cross sections, and the structural stiffness and pre- and post-yield strength of the femur diaphyses by pQCT and mechanical tests, and the gastrocnemius weight of rats that were either intact (n = 9) or Hx at 15 days of age (20). The latter were otherwise untreated (Hx controls, 4) or given 0.4 (8) or 2.0 (8) IU kg(-1) day(-1), s.c., of rhGH for 45 days starting 15 days after surgery. Hx delayed musculoskeletal development (gastrocnemius weight, bone geometric properties), thus affecting the diaphyseal stiffness and strength. It also reduced the cortical vBMD through an undefined mechanism, and increased the elastic modulus of cortical bone. The Hx also affected the correlation between bone geometric and material properties (xCSMI vs. E), suggesting an antianabolic interaction with the biomechanical control of bone modeling in response to strains caused by mechanical usage. As a result, Hx reduced the stiffness, post-yield, and ultimate strength of the diaphyses. These effects should reflect changes in bone tissue microstructure, perhaps associated with crack generation and progress, but unrelated to bone mineral mass. They are compatible with the induction of a delay in collagen turnover with associated increases in fibers' diameter and crystals' size that may have resulted from the suppression of some other hormones, such as thyroid, prolactin, or other hormones regulated by ACTH. The above doses of rhGH significantly but incompletely prevented the negative Hx effects on bone and muscle development (bone geometric properties, muscle mass). However, rhGH treatment failed to prevent the demineralizing and stiffening effect of Hx on bone tissue and the unusual effects on the post-yield strength (less clearly related to muscle development than the former). Consequently, rhGH treatment tended to preserve the natural relationship between muscle function and bone geometry but not bone strength. The effects of larger rhGH doses and the interaction of other hormones with the described effects remain to be investigated. Nevertheless, these findings would deserve special attention because they challenge the prevailing view that in endocrine-metabolic bone-weakening diseases the bone matrix always has a normal composition.

Aging↗