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Biomolecules and Tissue Properties
Published in Joseph W. Freeman, Debabrata Banerjee, Building Tissues, 2018
Joseph W. Freeman, Debabrata Banerjee
Tropoelastin contains both a-helix and beta sheet structures. Alanine and lysine rich segments lead to a-helices. Glycine-, proline-, and valine-rich segments lead to b-sheets. The a-helices form crosslinks because of lysine (allysine). Elastin is mainly found in the form of elastic fibers. Elastic fibers are composed of a large amorphous central core surrounded by a mesh of microfibrils. The core is composed of elastin, which gives elastic fibers a high capacity for stretch and recoil. Elastic fibers are formed through the deposit of tropoelastin onto a template of microfibrils, deposited by EBP. Microfibrils are composed of a mixture of several proteins including fibrillin. The microfibrils are oriented parallel to the direction of the applied force and are 10 nm wide, lying at the periphery of growing elastic fibers. Fibrillin is a glycoprotein that forms a sheath surrounding the amorphous elastin. Microfibrils are composed of end-to-end polymers of fibrillin.
Cell and Extracellular Matrix Interactions in a Dynamic Biomechanical Environment:
Published in Michel R. Labrosse, Cardiovascular Mechanics, 2018
As the name suggests, elastic fibers easily stretch under load and recoil to their original dimensions when unloaded. Elastic fibers are extremely stable, with a half-life of 40 years (Arribas et al. 2006), helping tissues maintain proper form when healthy, but they have limited repair mechanisms if damaged or degraded. Elastic fibers are macromolecules formed around a core of insoluble elastin, which makes up 90% of the fiber (Sherratt 2009). The other 10% consists of glycoproteins, most commonly fibrillin, in the form of microfibrils that surround the elastin. Like collagen, elastin is also formed by a complex cell-mediated process, whereby cells release the soluble precursor tropoelastin into the extracellular space, where tropoelastin molecules aggregate into coacervate (Czirok et al. 2006). Cellular motion aides the coacervate in assembling, crosslinking, and extending into elastic fibers.
Preclinical Models
Published in George C. Kagadis, Nancy L. Ford, Dimitrios N. Karnabatidis, George K. Loudos, Handbook of Small Animal Imaging, 2018
Irene Cuadrado, Jesús Egido, Jose Luis Zamorano, Carlos Zaragoza
Thoracic aortic aneurysm. Mouse models of disease contributed to significant progress in the understanding of thoracic aortic aneurysm (TAA). Marfan syndrome (MFS) is a common disorder of the connective tissue that involves the cardiovascular system and it is caused by mutations that affect the structure or expression of the extracellular matrix protein fibrillin-1, a glycoprotein that associates with extracellular proteins, including integrin receptors and insoluble elastin (Ramirez and Dietz 2007). Fibrillin-1 mutations in MFS decrease extracellular matrix sequestration of latent transforming growth factor-beta (TGFβ), thus rendering it more prone to or accessible for activation (Neptune et al. 2003; Habashi et al. 2006). TAA progression in MFS is driven by elastic fiber calcification, improper ECM proteins synthesis and matrix-degrading enzymes (matrix metalloproteinases), vascular wall inflammation, intimal hyperplasia, structural collapse of the vessel wall, as well as improper activation of MAP kinase signaling (Carta et al. 2009). In view of these results, systemic TGFβ antagonism is applied to mitigate vascular disease in mouse models of MFS and in children with severe and rapidly progressive MFS (Ramirez and Dietz 2007). In addition, murine models have recently shown that fibulin-4 and LRP1 are also associated to TAA (Boucher et al. 2007; Hanada et al. 2007).
Adverse cardiovascular effects of exposure to cadmium and mercury alone and in combination on the cardiac tissue and aorta of Sprague–Dawley rats
Published in Journal of Environmental Science and Health, Part A, 2021
Sandra Arbi, Megan Jean Bester, Liselle Pretorius, Hester Magdalena Oberholzer
Elastic fibers and SMC function together to allow the dilatory and constrictive action of the arterial wall, recoil ability of elastic blood vessels and ability to store energy. For elastin formation, the endothelial cells secrete soluble tropoelastin.[3,5] Pericellular deposited microfibrils composed of the protein fibrillin-1 serve as site of aggregation for soluble tropoelastin.[5] In the ECM, elastin is then cross-linked by lysyl oxidase (LOX) and lysyl oxidase like 1 (LOXL1), forming elastin fibers. These elastic fibers first appear as small cell surface globules which over time arrange themselves into larger fibers.[5] In hypertension, in addition to changes in collagen synthesis and deposition, the structure and the processing of elastin, fibrillin, fibronectin and proteoglycans are also altered.[3,5]
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
Elastin is accumulated on both edges of NAV, but is evenly distributed throughout HP. Elastin is responsible for the elastic properties of the NAV leaflet, and represents 13% of the total ECM dry weight [41]. Elastin is formed by lysyl oxidase crosslinking of tropoelastin monomers (~70 kDa), and it is surrounded by a fine mesh of microfibrils, predominantly fibrillin-1 and fibrillin-2 [52]. These fibrillins can bind integrins, proteoglycans and growth factors, and may play a role in cell signaling [53]. The elastin fibers in the lamina fibrosa of NAV form a highly-organized network of filaments that surround the collagen fiber bundles and stretch radially from the central region to the line of attachment of the leaflet. The elastin fibers store energy during the loading of the valve and release it to the collagen during unloading, thus allowing the valve to return to its resting position [54,55]. Elastin fibers in the ventricularis of NAV are responsible for the rapid retraction of the NAV leaflet in the radial direction during opening [41,42]. These fibers facilitate the closure movement by extending the valve leaflet as it opens, and they recoil when it closes [18,51]. They reduce the large radial strains that occur during maximum forward flow when NAV is opened. The elastin fibers in the lamina ventricularis of NAV also provide the mechanism for the pre-stress of the fibrosa by the ventricularis [18,51]. The benefit provided by this pre-stress is as yet unclear, but it is probably related to leaflet retraction. Stella et al. [49] showed that the elastin-rich ventricularis of the NAV leaflet contracted by 10.9% in the radial direction and by 8.2% in the circumferential direction, while the collagen-dominant fibrosa elongated by 28.2% in the radial direction and by 4.8% in the circumferential direction after layer separation. The elastin fibers of the lamina spongiosa are thicker in the hinge region of the NAV cusps, where they form a rectilinear pattern, as opposed to the thinner and radially oriented stripe pattern found in the middle part (belly region) of the cusps [56]. The elastin fibers in the lamina spongiosa probably play a role in responding to regionally specific loading patterns [56]. HP contained a smaller amount of elastin fibers than NAV. In addition, the elastin fibers have a different distribution in the individual layers of the HP tissue than in NAV. A denser concentration of elastin fibers was evident in the inner serosal part of the fibrous HP. In the HP, however, the elastin fibers were not arranged in such densely corrugated structures as were observed in the lamina ventricularis of NAV. Because of this, it can be assumed that they will have less effect on the elastic recoil and elastic recovery mechanisms in HP than in NAV. In addition, their contribution to providing the pre-stress mechanism during loading will be negligible in comparison with NAV.