scholarly journals Structure and function of the skeletal muscle extracellular matrix

2011 ◽  
Vol 44 (3) ◽  
pp. 318-331 ◽  
Author(s):  
Allison R. Gillies ◽  
Richard L. Lieber
2014 ◽  
Vol 2014 ◽  
pp. 1-15 ◽  
Author(s):  
Manoel Luís Costa

The function of muscle is to contract, which means to exert force on a substrate. The adaptations required for skeletal muscle differentiation, from a prototypic cell, involve specialization of housekeeping cytoskeletal contracting and supporting systems into crystalline arrays of proteins. Here I discuss the changes that all three cytoskeletal systems (microfilaments, intermediate filaments, and microtubules) undergo through myogenesis. I also discuss their interaction, through the membrane, to extracellular matrix and to other cells, where force will be exerted during contraction. The three cytoskeletal systems are necessary for the muscle cell and must exert complementary roles in the cell. Muscle is a responsive system, where structure and function are integrated: the structural adaptations it undergoes depend on force production. In this way, the muscle cytoskeleton is a portrait of its physiology. I review the cytoskeletal proteins and structures involved in muscle function and focus particularly on their role in myogenesis, the process by which this incredible muscle machine is made. Although the focus is on skeletal muscle, some of the discussion is applicable to cardiac and smooth muscle.


Biomaterials ◽  
2011 ◽  
Vol 32 (14) ◽  
pp. 3575-3583 ◽  
Author(s):  
Sara Hinds ◽  
Weining Bian ◽  
Robert G. Dennis ◽  
Nenad Bursac

2020 ◽  
Author(s):  
Reena Singh ◽  
Richard Tan ◽  
Clara Tran ◽  
Thomas Loudovaris ◽  
Helen E. Thomas ◽  
...  

2020 ◽  
Vol 118 (3) ◽  
pp. 258a
Author(s):  
Laszlo Csernoch ◽  
Mónika Gönczi ◽  
Zsolt Ráduly ◽  
László Szabó ◽  
Nóra Dobrosi ◽  
...  

1979 ◽  
Vol 82 (2) ◽  
pp. 227-234 ◽  
Author(s):  
VIPA BOONNAMSIRI ◽  
J. C. KERMODE ◽  
B. D. THOMPSON

SUMMARY Radio-iodide was administered by prolonged continuous intravenous infusion to rats maintained under iodine-replete conditions and in moderate iodine deficiency. A close approximation to equilibrium labelling was thereby achieved. Labelled iodocompounds extracted from various tissues were analysed by thin-layer chromatography. Moderate iodine deficiency resulted in a slight increase in the ratio of mono-iodotyrosine to di-iodotyrosine in the thyroid. No change in the ratio of tri-iodothyronine (T3) to thyroxine (T4) was found in thyroid, plasma or skeletal muscle. Faecal excretion of T3 declined appreciably relative to that of T4. Under iodine-replete conditions the ratio of thyroidal secretion rates of T3 and T4 was estimated to be more than three times higher than the ratio of these iodocompounds within the thyroid. Heterogeneity of thyroglobulin structure and function may explain these observations.


2006 ◽  
Vol 570 (3) ◽  
pp. 611-627 ◽  
Author(s):  
Giuseppe D'Antona ◽  
Francesca Lanfranconi ◽  
Maria Antonietta Pellegrino ◽  
Lorenza Brocca ◽  
Raffaella Adami ◽  
...  

1994 ◽  
Vol 14 (12) ◽  
pp. 8051-8057
Author(s):  
X Zhu ◽  
J E Yeadon ◽  
S J Burden

Although most skeletal muscle genes are expressed at similar levels in electrically active, innervated muscle and in electrically inactive, denervated muscle, a small number of genes, including those encoding the acetylcholine receptor, N-CAM, and myogenin, are expressed at significantly higher levels in denervated than in innervated muscle. The mechanisms that mediate electrical activity-dependent gene regulation are not understood, but these mechanisms are likely to be responsible, at least in part, for the changes in muscle structure and function that accompany a decrease in myofiber electrical activity. To understand how muscle activity regulates muscle structure and function, we used a subtractive-hybridization and cloning strategy to identify and isolate genes that are expressed preferentially in innervated or denervated muscle. One of the genes which we found to be regulated by electrical activity is the recently discovered acute myeloid leukemia 1 (AML1) gene. Disruption and translocation of the human AML1 gene are responsible for a form of acute myeloid leukemia. AML1 is a DNA-binding protein, but its normal function is not known and its expression and regulation in skeletal muscle were not previously appreciated. Because of its potential role as a transcriptional mediator of electrical activity, we characterized expression of the AML1 gene in innervated, denervated, and developing skeletal muscle. We show that AML1 is expressed at low levels in innervated skeletal muscle and at 50- to 100-fold-higher levels in denervated muscle. Four AML1 transcripts are expressed in denervated muscle, and the abundance of each transcript increases after denervation. We transfected C2 muscle cells with an expression vector encoding AML1, tagged with an epitope from hemagglutinin, and we show that AML1 is a nuclear protein in muscle. AML1 dimerizes with core-binding factor beta (CBF beta), and we show that CGF beta is expressed at high levels in both innervated and denervated skeletal muscle. PEBP2 alpha, which is structurally related to AML1 and which also dimerizes with CBF beta, is expressed at low levels in skeletal muscle and is up-regulated only weakly by denervation. These results are consistent with the idea that AML1 may have a role in regulating gene expression in skeletal muscle.


2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Viridiana Navarrrete ◽  
Marcos Ayala ◽  
Antonio Rodriguez ◽  
Francisco Villarreal ◽  
Israel Ramirez-Sanchez

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