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Mechanobiology of Heart Valves
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
Joshua D. Hutcheson, Michael P. Nilo, W. David Merryman
VECs have also been shown to play a role in the etiology and progression of valve disease. In diseased or injured vascular tissues, endothelial cells direct the appropriate immune response by upregulating cell adhesion molecules (CAMs) that mediate platelet attachment and activation, as well as by secreting cytokines that are recognized by specialized inflammatory cells.44–47 Similarly, AVECs have been observed to increase expression of CAMs (ICAM-1 and VCAM-1) and secretion of inflammatory cytokines such as IL-8, IL-1β and IFN-γ in response to oscillatory, turbulent fluid flows and pathological mechanical strains.60 The exact mechanisms by which the AVECs may contribute to pathogenesis in heart valves remain unclear; however, these cells may mediate tissue changes through paracrine signaling to the AVICs within the valve. In support of this theory, IL-1β has also been found in the cells within the valvular interstitium and may be important in modulating the overall disease progression.43
The Emergence of Order in Space
Published in Pier Luigi Gentili, Untangling Complex Systems, 2018
Also, the gradient mechanism is reasonably involved in the migration of cells. In fact, there is no doubt that some cells exhibit chemotaxis, meaning, cells receive signals from the surrounding tissues that direct them along the appropriate developmental pathway. During gastrulation, it is the difference in cell adhesion that guides the cells. In fact, change in cellular adhesiveness is another essential mechanism in the developmental program. The adhesiveness of a cell depends on specific proteins that are embedded in the cell’s surface membrane and have one portion that sticks out and binds to a similar or complementary molecule on adjacent cells. The crucial point is that cells express different Cell Adhesion Molecules (CAMs) at various stages in the development. CAMs play a pivotal role in the spatial arrangements of cells. The spatial organization of the different types of cells is essential for the formation of organs. Consider our arms and legs. Our arms and legs contain the same types of cells, such as muscle, tendon, skin, bone, and so on, yet they are different. The explanation lies in how these different types of cells arrange spatially. The differentiation of cells occurs through either environmental signals or unequal distribution of some special cytoplasmic factors at cell division.
Cell Adhesion in Animal Cell Culture: Physiological and Fluid-Mechanical Implications
Published in Martin A. Hjortso, Joseph W. Roos, Cell Adhesion, 2018
Manfred R. Koller, Eleftherios T. Papoutsakis
Aside from the relatively well-investigated mechanisms of cell attachment described above, many other cell surface receptors have been described in the literature. Many of these receptors are specific to certain types of cells and therefore do not lend themselves to a general discussion of cell attachment. Some examples of receptors for extracellular matrix components include: the 67-kDa laminin and elastin receptor (39), a different 67-kDa muscle-cell-specific laminin receptor (40), and chondrocyte-specific anchorin, which binds to collagen type II (41). Another type of molecule that is important in specific cell-cell interactions is the cell adhesion molecule (CAM). Many of these have been described in the literature, including the neural cell adhesion molecule (N-CAM) and the liver cell adhesion molecule (L-CAM). The CAMs are thought to play a major role in development by allowing cells to communicate with their neighbors, and they have been implicated in the induction of differentiation (for review see Ref. 42). Finally, one of the most important cell-cell interactions that has been studied is the tight junction that forms between epithelial cells. Tight junctions are restricted to these types of cells that are responsible for sealing body cavities. For example, epithelial cells of the intestinal lumen form tight junctions that completely encircle the cell and thereby form an impermeable seal between the intestinal lumen, which contains bacteria, and the internal abdominal cavity. These cell-cell interactions may be mimicked in vitro, and a variety of interesting culture systems, such as the growth of artificial skin, may result from this technology.
Exercise and inflammation in coronary artery disease: A systematic review and meta-analysis of randomised trials
Published in Journal of Sports Sciences, 2020
Gareth Thompson, Gareth W. Davison, Jacqui Crawford, Ciara M. Hughes
Exercise is an established therapeutic strategy for primary and secondary prevention of CAD (Alves et al., 2016; Anderson et al., 2016; Haskell et al., 2007; Piepoli et al., 2016). Interestingly, a meta-analysis performed by Swardfager et al. (2012) concluded that exercise may reduce inflammatory activity in CAD patients, as indicated by lower post-intervention values of C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6), and vascular cell adhesion molecule-1 (VCAM-1). As such, this conclusion suggests that exercise may induce an anti–inflammatory effect in CAD patients, which may partially represent a mechanism by which secondary prevention is conferred. However, the evidence produced by Swardfager et al. (2012) was generated by pooling randomised and non-randomised studies; the latter study design potentially decreasing the validity of the results due to selection bias (Reeves, Deeks, Higgins, & Wells, 2011). As such, this systematic review and meta-analysis will analyse randomised studies that investigated the effect of exercise on inflammatory biomarkers in CAD patients. Utilising this approach will provide a timely update to the evidence base by synthesising a rigorous examination of the capability of exercise to serve as an anti–inflammatory strategy in CAD.
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.
Polyphenon-E encapsulated into chitosan nanoparticles inhibited proliferation and growth of Ehrlich solid tumor in mice
Published in Egyptian Journal of Basic and Applied Sciences, 2018
Azza I. Othman, Ibrahim M. El-Sherbiny, Mohamed A. ElMissiry, Doaa A. Ali, Engy AbdElhakim
Tumor tissues were fixed in 10% neutral-buffered formalin, and embedded in paraffin and 5 μm sections were prepared for staining. The proliferating cell nuclear antigen (PCNA), platelet endothelial cell adhesion molecule-1 (PCAM/CD31) and vascular endothelial growth factor (VEGF) were obtained from ThermoFisher Scientific, USA with the following specifications; (PCNA, Mouse monoclonal antibody, MS-106-P0, USA), (CD31, rabbit polyclonal antibody, RB-10333-R7) and (VEGF, rabbit polyclonal antibody, RB-9031-R7). Immunohisochemical studies were performed by incubating tumor sections with suitable dilutions 1:50–1:400 primary antibodies. Negative control sections were prepared without primary antibody. All tissue sections were inspected using light microscopy to obtain images using Olympus (IX51) microscope [25].