Arteries elastic tissue

According to Loeper et al., who have studied the role of silicon in human and experimental atherosclerosis6 7 silicon has a protective function for the artery by decreasing the atheromatous deposits and by conserving the integrity of the elastic tissue and the connective tissue. 

The form in which elastin is laid down varies considerably in the different types of elastic tissue. Membranes with a very high elastin content are found in the walls of the larger arteries, in some parts of the heart, and in the trachea and bronchi. In the larger arteries the structural units of the elastic tissue formation are concentric lamellae which are often of rather variable thickness and always contain many irregular openings. In the ligamentum nuchae of some animals, particularly the ox, the structure is quite different and thick longitudinal elastic fibers, of almost circular cross section, form most of the tissue. 

Diseases of elastic tissue are few compared with those that affect collagen, and in these destruction of preformed elastic fibers appears to occur only in localized areas, particularly in the walls of blood vessels and in the skin. In arteriosclerosis loss of elasticity and breakdown in the structure of the elastic elements in the media of arteries is accompanied by calcification of the media and the development of calcified plaques in the intima. Since calcification of the media may be seen to occur without the development of atheromata, it is thought that this change may be associated in the first place with age. Other age-related changes looked for have been changes in the gross content of elastin in the media and changes in the amino acid... 

The turnover rate of mature elastin in healthy persons is relatively low. Insoluble elastin in healthy elastic tissue is usually stable and subjected to minimal proteolytic degradation. In several clinical conditions (e.g., emphysema, advanced atherosclerosis, pancreatitis), increased degradation of fragmentation of elastic fibers may play a significant role. The interaction between insoluble elastin and soluble elastolytic enzymes, and the regulation of these enzymes, may shed light on certain cardiovascular diseases, in view of the role of elastin in arterial dynamics. 

In the normal adult, the different histological, electrophysiological, biochemical, immunochemical and pharmacological properties displayed by the various SM tissues and cells might be tentatively typified in a SM tree (Fig. 1 see also text ahead). As far as the arterial SM tissue is concerned, the end-point of this classification tree is represented by the two wall layers the intima and the media [7]. The intima is composed of a single layer of endothelial cells, the subendothelial membrane and the internal elastic... 

In other cases, where elastin serves in ECM to control cell and matrix function, elastin has lesser tropoelastin chains and, along with collagen, plays very important roles in the regulation of cells, especially in elastic tissues such as blood vessels [96]. Several studies have shown the roles of elastin during arterial morphogenesis, via knockout experiments. Significant differences in SMC proliferation were observed in cases where tropoelastin was knocked out [96,97]. In another study, elastin knockout mitigated SMC proliferation and the effect was shown to be dose-dependent [98]. Similar effects have been demonstrated in other studies with endothelial cells [99]. Cell proliferation and differentiation was reduced due to elastin knockout. Several other studies have also shown very similar effects with dermal fibroblasts, where elastin plays a very important role in the matrix as a defense mechanism as described earlier. Dermal fibroblasts failed to attach and proliferate on the elastin deprived matrices [89,100]. 

A protein that is similar to collagen is elastin, which is present in elastic tissues, such as tendons and arteries. Hydrolyses of elastin, which has rubber-like properties, however, do not yield gelatin. Mildly hydrolyzed elastin can be fractionated into two proteins. ... 

The structure of the venous walls is basically similar to that of the arterial walls. The main difference is that they contain less muscle and elastic tissue than the arterial walls, which raises the static elastic modulus two to fourfold [49]. Because the venous walls are much thinner than the arterial wall, they are easily collapsible when they are subject to external compressions. 

Elastin is the protein found in elastic tissues such as tendons and arteries. The polypeptide chain of elastin is rich in alanine and glycine and is very flexible. It contains cross-links involving lysine side chains, which prevent the protein from extending excessively under tension and allow it to return to its normal length when tension is removed. 

The first elastomeric protein is elastin, this structural protein is one of the main components of the extracellular matrix, which provides stmctural integrity to the tissues and organs of the body. This highly crosslinked and therefore insoluble protein is the essential element of elastic fibers, which induce elasticity to tissue of lung, skin, and arteries. In these fibers, elastin forms the internal core, which is interspersed with microfibrils [1,2]. Not only this biopolymer but also its precursor material, tropoelastin, have inspired materials scientists for many years. The most interesting characteristic of the precursor is its ability to self-assemble under physiological conditions, thereby demonstrating a lower critical solution temperature (LCST) behavior. This specific property has led to the development of a new class of synthetic polypeptides that mimic elastin in its composition and are therefore also known as elastin-like polypeptides (ELPs). 

Another noteworthy anatomical feature of the arteries is the presence of elastic connective tissue. When the heart contracts and ejects the blood, a portion of the stroke volume flows toward the capillaries. However, much of the stroke volume ejected during systole is retained in the distensible arteries. When the heart relaxes, the arteries recoil and exert pressure on the blood within them, forcing this "stored" blood to flow forward. In this way, a steady flow of blood toward the capillaries is maintained throughout the entire cardiac cycle. 

As the arteries travel toward the peripheral organs and tissues, they branch and become smaller. Furthermore, the walls of the vessels become less elastic and more muscular. The smallest arterial vessels, arterioles, are composed almost entirely of smooth muscle with a lining of endothelium. 

Due to the significant amount of elastic connective tissue and smooth muscle in their walls, arteries tend to recoil rather powerfully, which keeps the pressure within them high. In contrast, veins contain less elastic connective tissue and smooth muscle so the tendency to recoil is significantly less and the pressure remains low. 

Function and location of elastin Cause of Marfan syn drome Elastin is a connective tissue protein with rubber-like properties. Elastic fibers composed of elastin and glycoprotein microfibrils, such as fibrillin, are found in the lungs, the walls of large arteries, and elastic ligaments. [Note Mutations in the fibrillin gene are responsible for Marfan syndrome]... 

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