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Results for “Myocytes, Smooth Muscle”

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PubMed2003

Maturation of the regulation of GLUT4 activity by p38 MAPK during L6 cell myogenesis.

Insulin stimulates glucose uptake in skeletal muscle cells and fat cells by promoting the rapid translocation of GLUT4 glucose transporters to the plasma membrane. Recent work from our laboratory supports the concept that insulin also stimulates the intrinsic activity of GLUT4 through a signaling pathway that includes p38 MAPK. Here we show that regulation of GLUT4 activity by insulin develops during maturation of skeletal muscle cells into myotubes in concert with the ability of insulin to stimulate p38 MAPK. In L6 myotubes expressing GLUT4 that carries an exofacial myc-epitope (L6-GLUT4myc), insulin-stimulated GLUT4myc translocation equals in magnitude the glucose uptake response. Inhibition of p38 MAPK with SB203580 reduces insulin-stimulated glucose uptake without affecting GLUT4myc translocation. In contrast, in myoblasts, the magnitude of insulin-stimulated glucose uptake is significantly lower than that of GLUT4myc translocation and is insensitive to SB203580. Activation of p38 MAPK by insulin is considerably higher in myotubes than in myoblasts, as is the activation of upstream kinases MKK3/MKK6. In contrast, the activation of all three Akt isoforms and GLUT4 translocation are similar in myoblasts and myotubes. Furthermore, GLUT4myc translocation and phosphorylation of regulatory sites on Akt in L6-GLUT4myc myotubes are equally sensitive to insulin, whereas glucose uptake and phosphorylation of regulatory sites on p38 MAPK show lower sensitivity to the hormone. These observations draw additional parallels between Akt and GLUT4 translocation and between p38 MAPK and GLUT4 activation. Regulation of GLUT4 activity by insulin develops upon muscle cell differentiation and correlates with p38 MAPK activation by insulin.

Animals↗
PubMed1962

Centrioles and the formation of rudimentary cilia by fibroblasts and smooth muscle cells.

Cells from a variety of sources, principally differentiating fibroblasts and smooth muscle cells from neonatal chicken and mammalian tissues and from organ cultures of chicken duodenum, were used as materials for an electron microscopic study on the formation of rudimentary cilia. Among the differentiating tissues many cells possessed a short, solitary cilium, which projected from one of the cell's pair of centrioles. Many stages evidently intermediate in the fashioning of cilium from centriole were encountered and furnished the evidence from which a reconstruction of ciliogenesis was attempted. The whole process may be divided into three phases. At first a solitary vesicle appears at one end of a centriole. The ciliary bud grows out from the same end of the centriole and invaginates the sac, which then becomes the temporary ciliary sheath. During the second phase the bud lengthens into a shaft, while the sheath enlarges to contain it. Enlargement of the sheath is effected by the repeated appearance of secondary vesicles nearby and their fusion with the sheath. Shaft and sheath reach the surface of the cell, where the sheath fuses with the plasma membrane during the third phase. Up to this point, formation of cilia follows the classical descriptions in outline. Subsequently, internal development of the shaft makes the rudimentary cilia of the investigated material more like certain non-motile centriolar derivatives than motile cilia. The pertinent literature is examined, and the cilia are tentatively assigned a non-motile status and a sensory function.

Animals↗
PubMed1957

The structure of the smooth muscle fibres in the body wall of the earth worm.

1. The structure of the smooth muscle fibres in the longitudinal muscle coat of the body wall of Lumbricus terrestris has been investigated by phase contrast light microscopy and electron microscopy. 2. The muscle fibre is ribbon-shaped, and attached to each of its two surfaces is a set of myofibrils. These are also ribbon-shaped, and they lie with their surfaces perpendicular to the surfaces of the fibre, and their inner edges nearly meeting in the middle of the fibre. These fibrils are oriented at an angle to the fibre axis, and diminish greatly in width as they approach the edge of the fibre. The orientation of the set of fibrils belonging to one surface of the fibre is the mirror image of that of the set belonging to the other surface; thus, when both sets are in view in a fibre lying flat on one face, the fibre exhibits double oblique striation. A comparison of extended and contracted fibres indicates that as the fibre contracts, the angle made between fibre and fibril axes increases (e.g. from 5 to 30 degrees ) and so does the angle made between the two sets of fibrils (e.g. from 10 to 60 degrees ). 3. The myofibril, throughout its length, contains irregularly packed filaments, commonly 250 A in diameter, which are parallel to its long axis and remain straight in contracted muscles. Between them is material which probably consists of much finer filaments. Thus A and I bands are absent. 4. Bound to one face of each fibril, but not penetrating inside it, is a regularly spaced series of transverse stripes. They are of two kinds, alternating along the length of the fibril, and it is suggested that they are comparable to the Z and M lines of a cross-striated fibril. The spacing of these stripes is about 0.5 micro ("Z" to "Z") in extended muscles, and 0.25 micro in contracted muscles. A bridge extends from each stripe across to the stripeless surface of the next fibril.

Animals↗
PubMed2002

Alterations in endothelial cell proliferation and apoptosis contribute to vascular remodeling following hind-limb ischemia in rabbits.

Hind-limb ischemia is a potent stimulus for angiogenesis. However, capillary density does not change in tibialis anterior muscle (TA) following hind-limb ischemia, despite increases in angiogenic growth factors. The objective of this study was to determine whether changes in proliferation and apoptosis occurred in the same muscle. In total, 19 New Zealand white rabbits underwent femoral artery ligation and excision and the ischemic and contra-lateral (control) TA muscles were harvested after 1 (n = 7), 5 (n = 7) and 21 (n= 5). Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) was used to detect apoptosis and double staining was used to identify the apoptotic cell types. Proliferation was assessed by immunohistochemistry for proliferating cell nuclear antigen (PCNA) and [3H]thymidine incorporation, in vitro. TUNEL positive nuclei were greater in ischemic than control muscle at 1 day (1.83 +/- 0.70% vs 1.03 +/- 0.20%), 5 days (2.13 +/- 0.50% vs 1.21 +/- 0.42%) and at 21 days the difference was statistically significant (3.42 +/- 0.80% vs 0.96 +/- 0.40%, p < 0.01). The majority of TUNEL positive nuclei were endothelial (Tie2 positive) cells. The number of PCNA positive cells in ischemic versus control muscle was similar at 1 day (0.71 +/- 0.20% vs 0.53 +/- 0.20%) and 5 days (1.28 +/- 0.30% vs 0.77 +/- 0.30%), but was significantly (p < 0.05) reduced in ischemic muscle at 21 days (0.18 +/- 0.20% vs 1.35 +/- 0.30%) with no difference in [3H]thymidine incorporation. Directionally opposite changes in endothelial cell proliferation and apoptosis occur in TA muscle following hind-limb ischemia. Modulating apoptosis in ischemic skeletal muscle may present a novel therapeutic target in peripheral arterial disease.

Animals↗
PubMed2005

Fgf10 expression identifies parabronchial smooth muscle cell progenitors and is required for their entry into the smooth muscle cell lineage.

Lineage formation in the lung mesenchyme is poorly understood. Using a transgenic mouse line expressing LacZ under the control of Fgf10 regulatory sequences, we show that the pool of Fgf10-positive cells in the distal lung mesenchyme contains progenitors of the parabronchial smooth muscle cells. Fgf10 gene expression is slightly repressed in this transgenic line. This allowed us to create a hypomorphic Fgf10 phenotype by expressing the LacZ transgene in a heterozygous Fgf10 background. Hypomorphic Fgf10 mutant lungs display a decrease in beta-galactosidase-positive cells around the bronchial epithelium associated with an accumulation of beta-galactosidase-expressing cells in the distal mesenchyme. This correlates with a marked reduction of alpha smooth muscle actin expression, thereby demonstrating that FGF10 is mostly required for the entry of mesenchymal cells into the parabronchial smooth muscle cell lineage. The failure of exogenous FGF10 to phosphorylate its known downstream targets ERK and AKT in lung mesenchymal cultures strongly suggests that FGF10 acts indirectly on the progenitor population via an epithelial intermediate. We provide support for a role of epithelial BMP4 in mediating the formation of parabronchial smooth muscle cells.

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