Platelets and Thrombosis in the Development of Atherosclerosis and Its Complications

Mustard, J. F.; Packham, Marian A.; Kinlough-Rathbone, R L

doi:10.1007/978-1-4757-1217-9_2

Cited by 33 publications

(9 citation statements)

References 74 publications

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“…The activated platelets interact with the surface of the FL wall and further release factors that contribute to the accumulation of platelets at an injury site, thereby accelerating FL thrombosis. 48 Another widely used WSS index is oscillatory shear index (OSI). High OSI values are found to coincide with areas of low TAWSS in our study, which is comparable to Alimohammadi et al 16 However, the locations of high OSI/low TAWSS regions are different in our study due to differences in model geometry and the extent of flap motion.…”

Section: Effect Of Flap Motion On Wssmentioning

confidence: 99%

Effect of intimal flap motion on flow in acute type B aortic dissection by using fluid‐structure interaction

Chong

Chan

et al. 2020

Numer Methods Biomed Eng

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A monolithic, fully coupled fluid-structure interaction (FSI) computational framework was developed to account for dissection flap motion in acute type B aortic dissection (TBAD). Analysis of results included wall deformation, pressure, flow, wall shear stress (WSS), von Mises stress and comparison of hemodynamics between rigid wall and FSI models. Our FSI model mimicked realistic wall deformation that resulted in maximum compression of the distal true lumen (TL) by 21.4%. The substantial movement of intimal flap mostly affected flow conditions in the false lumen (FL). Flap motion facilitated more flow entering the FL at peak systole, with the TL to FL flow split changing from 88:12 in the rigid model to 83:17 in the FSI model. There was more disturbed flow in the FL during systole (5.8% FSI vs 5.2% rigid) and diastole

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Section: Effect Of Flap Motion On Wssmentioning

confidence: 99%

Effect of intimal flap motion on flow in acute type B aortic dissection by using fluid‐structure interaction

Chong

Chan

et al. 2020

Numer Methods Biomed Eng

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“…Under standard experimental conditions, the adhesion reached its plateau after 40 min of incubation. The number of adherent platelets was a linear function of platelet count in the range 1 (Fig. 1E), platelet adhesion to the surface of ECs was low (0.9 + 0.3 x 103/mm2, mean + SEM; n = 4).…”

mentioning

confidence: 94%

“…The injury or loss of endothelial cells (ECs) results in the loss of athrombogenic properties by the vessel wall and this leads to adhesion of blood platelets to the injured surface. It is thought that the recognition of injury occurs through a specific interaction of platelets with subendothelium, of which several constituents, particularly collagen, have high affinity toward platelets (1,2).…”

mentioning

confidence: 99%

Endothelial cell culture on fibrillar collagen: model to study platelet adhesion and liposome targeting to intercellular collagen matrix.

Чазов¹,

Alexeev²,

Antonov³

et al. 1981

Proc. Natl. Acad. Sci. U.S.A.

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Human umbilical endothelial cells (ECs) were grown on fibrillar type I collagen in 16.4-mm multiwell tissue culture plates. Human platelets were added to the wells, and platelet adhesion to collagen was examined by scanning electron microscopy and radioisotopic technique in the absence of ECs and in preconfluent and confluent EC cultures. Single adherent platelets of different shapes as well as small aggregates were seen on collagen surface. Human plasma fibronectin added to the system stimulated platelet adhesion and their spreading on collagen. ECs had no effect on the percentage of platelets adherent to collagencoated gaps in preconfluent culture but decreased the number of spread platelets. It is demonstrated that collagen-coated gaps can bind ' C-labeled liposome.antibody and "'C-labeled liposome-fibronectin conjugates. ECs grown on fibrillar collagen are suggested as useful models for screening of antiplatelet drugs and for the study of drug targeting tothe areas of vascular injury for prevention of thrombosis..At present, injury of the endothelial lining of the vessel wall is viewed as one of the key mechanisms of thrombogenesis and, possibly, ofatherogenesis (for review, see refs. 1-3). The injury or loss of endothelial cells (ECs) results in the loss of athrombogenic properties by the vessel wall and this leads to adhesion of blood platelets to the injured surface. It is thought that the recognition of injury occurs through a specific interaction of platelets with subendothelium, of which several constituents, particularly collagen, have high affinity toward platelets (1, 2).To study the mechanism of platelet adhesion to the injured vessel wall, everted vessel segments or surfaces coated with fibrillar collagen have been used (2, 4-6). In the work reported here, an experimental model is described which includes partial reconstitution of the luminal surface of "normal" and "injured" vessel wall. This surface is imitated by a bilayer structure of confluent or preconfluent EC cultures grown on fibrillar collagen. The model was used for: (i) quantitative studies ofplatelet adhesion to collagen-coated gaps in preconfluent EC cultures and to the surface of ECs; (ii) examination of effects produced by plasma fibronectin and ECs on the adhesion and spreading ofplatelets on fibrillar collagen; and (iii) attempts to develop an approach for specific recognition ofcollagen-coated gaps in preconfluent EC culture by "4C-labeled liposome-antibody to type I collagen andd "4C-labeled liposome-fibronectin conjugates. MATERIALS AND METHODSIsolation of Fibronectin, Collagen, and Antibodies to Collagen. Human plasma fibronectin was isolated by affinity chromatography on gelatin-Sepharose (7) 5603The publication costs ofthis article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U. S. C. §1734 solely to indicate this fact.

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“…When endothelium is removed from the aortic wall, platelets immediately adhere to the exposed subendothelium, forming a carpetlike layer covering the entire luminal surface (15)(16)(17). However, if similar de-endothelialized areas are examined several days after endothelial removal, relatively few platelets adhere to the vascular surface (18,19).…”

Section: Introductionmentioning

confidence: 99%

Recovery of prostacyclin production by de-endothelialized rabbit aorta. Critical role of neointimal smooth muscle cells.

Eldor¹,

Falcone²,

Hajjar³

et al. 1981

J. Clin. Invest.

166

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A B S T R A C T Prostacyclin (PGI2) synthetic capacity was assayed at the surface of aortas at various intervals after removal of endothelium with a balloon catheter. Results were correlated with morphologic changes in the vessel wall seen by light microscopy, scanning and transmission electron microscopy. To assay PGI2 synthetic capacity, we applied an incubation chamber to the luminal surface of the aortas; after arachidonic acid stimulation we assayed the PGI2 synthesized with a bioassay and radioimmunoassay. PGI2 synthesis in deendothelialized aortas was determined immediately after balloon-catheter injury and at intervals of 1 h and 2, 4, 15, 35, and 70 d. PGI2 synthesis was low at 1 h and increased over time with levels at 35 and 70 d reaching that of normal artery. Scanning and transmission electron microscopy of de-endothelialized areas showed persistent absence of endothelium with formation of a neointima composed of smooth muscle cells. De-endothelialized aorta was covered with adherent platelets shortly after injury, however several days later only a few platelets adhered to the denuded surface.Results indicated that (a) endothelium is responsible for nearly all PGI2 production at the luminal surface of the normal aorta, (b) de-endothelialized muscular neointima synthesized increasing quantities of PGI2 with time after injury, and (c) increase of PGI2

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Platelets and Thrombosis in the Development of Atherosclerosis and Its Complications

Cited by 33 publications

References 74 publications

Effect of intimal flap motion on flow in acute type B aortic dissection by using fluid‐structure interaction

Effect of intimal flap motion on flow in acute type B aortic dissection by using fluid‐structure interaction

Endothelial cell culture on fibrillar collagen: model to study platelet adhesion and liposome targeting to intercellular collagen matrix.

Recovery of prostacyclin production by de-endothelialized rabbit aorta. Critical role of neointimal smooth muscle cells.

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