Vitronectin in atherosclerotic disease

Lack of Complement Inhibitors in the Outer Intracranial Artery Aneurysm Wall Associates with Complement Terminal Pathway Activation

“…This suggests that part of the terminal complexes could be in the soluble form SC5b-9. Clusterin and vitronectin, however, also have potential functions (eg, in vascular remodeling) [25][26] in addition to inhibition of MAC assembly on the cell membrane. Therefore clusterin and vitronectin could have additional roles in the IAs.…”

Endovascular Histologic Effects of Ultrathin Gold- or Vitronectin-Coated Platinum Aneurysm Coils in a Rodent Arterial Occlusion Model: A Preliminary Investigation

“…[31][32][33][34] It is capable of forming complexes with plasminogen activator inhibitor, thrombin-antithrombin III, and complement C5b-C9, with consequent conformational changes that expose the heparinbinding site on vitronectin. 38,39 It has complex and incompletely explored roles in the regulation of thrombosis and fibrinolysis, 40,41 pericellular proteolysis, cell attachment, and complement-dependent immune response.…”

“…[28][29][30] Vitronectin, a plasma glycoprotein that plays a role in platelet activation, has been demonstrated to increase the platelet coating of biopolymers. [31][32][33][34][35][36] Despite these favorable characteristics of gold and vitronectin for the treatment of cerebral aneurysms, no experiments to date have investigated the potential utility of applying these materials to standard platinum aneurysm coils. The purpose of this initial preliminary study, therefore, was to evaluate the degree of neointimal change associated with ultrathin gold-or vitronectin-coated platinum coils in a rodent model of saccular aneurysms.…”

Modern view on the structure of the vascular extracellular matrix

“…These fibrils, composed largely of type VII collagen, extend from the lamina densa and wrap around the collagen fibers or directly attach to it over anchoring plates thus connecting the collagen fibers to the fibronectin (18,19). With electron microscopy, lamina densa can be seen as a continuous layer, 80 nm thin (37). All components of the basal lamina are produced by endothelial cells except the fibronectin that can be produced by connective tissue cells as well (20,21).…”

“…Vitronectin is also involved in cellular migration through αvβ3 and αvβ3 integrins (36), while osteopontin shows great affinity for collagen and promotes migration of the smooth muscle cells during atherosclerosis. Osteopontin enhances the development of fatty streaks in mice on high cholesterol diet which suggests its role in the plaque formation (37,38).…”