Library Lambak Kanan

Depending on the location in the body, the vessels diameter and function, and the amounts of BM and ECM of the vasculature, its phenotype and composition may vary.Together these are sometimes known as the tunica intima.The central layer, the tunica media, is primarily smooth muscle and elastic bers and is usually the thickest.The outermost layer, which attaches the vessel to the surrounding tissue, is called the tunica adventitia, and is made up of connective tissue with varying amounts of elastic and collagenous bers.Mathematical modeling of tumorinduced angiogenesis have a lifetime ranging from months to years.They are also selectively permeable for small peptides and proteins, and also regulate blood coagulation via the synthesis of thrombomodulin, tissue factor. The deposition of provisional ECM components is also important for EC migration and survival during angiogenesis.The ECM is comprised of three main types of molecules: specialized proteins such as brillin, bronectin, vitronectin, and laminin, and proteoglycans, which consist of a Icariin protein core surrounded by attached long chains of repeating units.Collagens, which occur in at least a dozen forms, provide tensile strength and elasticity to the ECM.Fibronectins are large glycoproteins which are assembled from two brous polypeptides; they are found in basal laminae and in the loose connective tissue underneath the skin and between the body organs.Laminin is a large crossshaped glycoprotein which is constructed from three polypeptides.These molecules are primarily linkers in networks and anchors that attach cells to basal laminae.In vertebrates proteoglycans occur wherever collagens occur in the ECM.Individual proteoglycans can link to collagen bers, thereby forming the bernetwork complex of the ECM.Proteoglycans also function as sites for cell adhesions, both temporary and permanent.Localized degradation of the basement membrane requires the expression of proteases that are specic for the resident ECM, and the concomitant expression of protease inhibitors to prevent excess matrix degradation and loss of tissue integrity.Recent studies in a variety of tumors have shown that tumor cells stimulated by hypoxia start secreting some of these angiogenic factors.These factors stimulate EC growth and migration, and have different effects on EC expression of proteases that degrade the ECM, such as the plasminogen activator. The best known of these growth factors are transforming growth factor beta, which is also called vascular permeability factor. These factors activate specic cell surface receptors, which in turn activate intracellular signal transduction pathways.TGF is a member of the growth factor family that acts on some cells to stimulate cell proliferation and others to inhibit it, or stimulates at one concentration and inhibits at another.However, LTGF can be converted into the Harmine active form by the protease plasmin. Interestingly, active TGF has been found to induce the synthesis of plasminogen activator inhibitor, which blocks the conversion of plasminogen to plasmin. Thus, the activation of LTGF is a selfregulating system, since plasmin formation increase leads to enhanced conversion of LTGF to TGF. However, more TGF induces PAI synthesis, thereby reducing plasmin formation, and with less plasmin, conversion of LTGF to TGF decreases and PAI synthesis will fall, which allows plasmin formation to increase and the cycle starts over again bFGF is a multifunctional growth factor present in several tissues in vivo and is synthesized by a number of cell types in vitro.

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