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Functional Properties of Muscle
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Smooth muscle cells are relatively small and spindle-shaped, being 2–10 µm in diameter 20–500 µm in length, with a single nucleus (Figure 10.22). Smooth muscle is so called because it is non-striated, the thick and thin filaments are not organized into myofibrils, and there are no aligned sarcomeres to produce striations. Instead, the thick filaments are scattered throughout the cell, and the organization of their myosin is different from that in skeletal and cardiac muscle. The thin filaments are connected to dense bodies, which are functionally similar to the Z discs of skeletal muscle. The dense bodies are part of a filamentous network that is firmly attached to the cell membrane and composed mainly of the protein desmin. Thus, when the thick and thin filaments slide past one another, force is transmitted to the cell membrane. However, the unorganized arrangement of thick and thin filaments allows the development of force over a range of lengths that can be four times that in skeletal muscle. The amount of myosin in smooth muscle, in mg/g of muscle, is roughly a third to a quarter of that in skeletal muscle, while the amount of actin can be up to twice as much.
Adult Stem Cell Plasticity
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Others confirmed these results using untreated MSC in different animal models. MSC expanded and chemically labeled in culture integrated into cardiac muscle when injected into healthy myocardium.108 Labeled cells were aligned in intercalated disks, exhibited myocyte morphology, and stained positively for connexin 43. The presence of this component of gap junctions indicates that the donor-derived cells were electrically coupled to the endogenous myocardium. When human MSC, transfected with the LacZ gene, were injected into the uninjured myocardium of immunodeficient mice, LacZ+ cells were found within four days.109 Although these did not initially express protein markers of cardiac muscle, after fourteen days, donor cells were rod shaped and aligned with other cardiomyocytes, had increased in size, and expressed desmin, cardiac troponin T, α-actinin, phospholamban, and β-myosin heavy chain. Unfortunately, engraftment rates were low in both these studies; only about 1 LacZ+ cell per tissue section was found by Toma et al.
Bladder Tissue Engineering
Published in Gilson Khang, Handbook of Intelligent Scaffolds for Tissue Engineering and Regenerative Medicine, 2017
Stem cells obtained from (voided) urine might also provide an alternative cell source for bladder tissue engineering. The phenotype of urine cells harvested from the upper urinary tract is similar to mesenchymal stromal cells: CD29, CD44, CD54, CD73, CD90, CD105, CD166, and STRO-1-positive.81,82 These cells can be differentiated into urothelial cells (uroplakin+, cytokeratin 7+, and cytokeratin 13+) and smooth muscle cells (α-SMA+, desmin+, and myosin+). Urine-derived stem cells showed a remarkable capacity to expand. Up to 60–70 population doublings were noted, and cells had detectable telomerase activity and long telomeres, which suggests that they represent progenitor cells. When cells derived from voided urine were seeded on scaffolds multilayered tissue like structures formed after implantation in nude mice.82 In an alternative approach multilayered urothelial sheets were prepared from urothelial cells obtained after bladder washes. Samples from bladder cancer patients were excluded. Mesenchymal α-SMA+ cells were excluded, because the aim of this study was to create multilayers of urothelia. The harvested cells formed a monolayer and by applying cell sheets and inducing cells with increased Calcium, urothelial cells stratified in vitro. The stratified cell culture consisted of a superficial urothelial cell layer (CK20+) and a basal cell layer (p63+). The investigators suggested that this multilayered urothelial sheet could be applied as flaps in open urethral surgery and that such multilayered sheets might be useful in endoscopic urethroplasty.83
A human pericardium biopolymeric scaffold for autologous heart valve tissue engineering: cellular and extracellular matrix structure and biomechanical properties in comparison with a normal aortic heart valve
Published in Journal of Biomaterials Science, Polymer Edition, 2018
Frantisek Straka, David Schornik, Jaroslav Masin, Elena Filova, Tomas Mirejovsky, Zuzana Burdikova, Zdenek Svindrych, Hynek Chlup, Lukas Horny, Matej Daniel, Jiri Machac, Jelena Skibová, Jan Pirk, Lucie Bacakova
Immunohistochemical detection of collagen I, III and elastin was performed on paraffin sections 4 μm in thickness, using a two-step indirect method. The slides were deparaffinized in xylene, and were rehydrated in graded ethanol. After deparaffinization and rehydration, endogenous peroxidase was blocked by 0.3% H2O2 in 70% methanol for 30 min. A primary antibody was applied for 30 min at RT, and antibody detection was performed using Histofine Simple Stain MAX PO (MULTI) Universal Immuno-peroxidase Polymer, anti-Mouse and anti-Rabbit (Histofine; Nichirei, Japan). Immunohistochemical detection of vimentin (a type III intermediate filament protein), desmin (a marker of striated muscles), alpha smooth muscle actin (α-SMA), Ki-67 (a nuclear marker for cell proliferation), CD31 (a platelet-endothelial cell adhesion molecule, also referred to as PECAM-1), leukocyte common antigen (LCA) and β-catenin (a cell adhesion protein associated with cadherin junctions linking cadherins to the actin cytoskeleton) were performed on sections of paraffin-embedded tissues 4 μm in thickness, using the Ventana Benchmark Ultra system (Tuscon, AZ, USA) with the ultraView Universal DAB Detection Kit.
The stiffness response of type IIa fibres after eccentric exercise-induced muscle damage is dependent on ACTN3 r577X polymorphism
Published in European Journal of Sport Science, 2019
Siacia Broos, Laurent Malisoux, Daniel Theisen, Ruud Van Thienen, Marc Francaux, Martine A. Thomis, Louise Deldicque
In search for likely differences between RR and XX genotypes in the responses to eccentric exercise, intramuscular markers were quantified both at the protein and at the mRNA levels. No difference was measured in any marker at baseline between the two groups. The mRNA level of MyoD1, myogenin, XIRP1, STARS1, ATF3 and RCAN1 were increased 5 h after the eccentric exercise bout of the quadriceps. Yet, the increase was similar in both genotype groups for all markers tested, except for NFATc1. The latter showed a lower expression in the XX group after the exercise bout but remained unchanged in the RR genotypes. NFATc1 has been linked to hypertrophy and is required for fast-to-slow fibre type switching in response to exercise (Ehlers, Celona, & Black, 2014). A decreased NFATc1 mRNA content led to a lower percentage of slow fibres and an increased fast fibre gene expression in mice following a 7-day period of voluntary exercise. As α-actinin-3 deficient muscles are known to harbour a lower percentage of fast fibres (Vincent et al., 2007), the decreased NFATc1 mRNA content in XX genotypes in this study was at least unexpected. Unfortunately, based on previous reports and the present results, the decreased NFATc1 levels after eccentric exercise in the XX group cannot be explained. Protein expressions of myotilin, ZASP, vinculin and desmin were unaltered 5 h post-exercise. The time-course of the inflammatory response depends on several factors such as the muscle group used, type of contractions and study protocol (type, intensity, duration of the exercise) (MacIntyre, Reid, & McKenzie, 1995), which could explain why other studies did observe a change in protein levels 5 h after an exercise bout (Mitchell et al., 2013). These results led us to conclude that ACTN3 R577X polymorphism had no effect on intramuscular markers for muscle damage and regeneration 5 h after an eccentric exercise bout of the quadriceps.