scholarly journals THROMBOCYTOPATHIES IN CHILDREN WITH IMPAIRED PLATELET ADHESION AND AGGREGATION

2020 ◽  
pp. 26-29
Author(s):  
B.E. Isaeva ◽  
E.K. Makimbetov
Keyword(s):  
Platelet Adhesion ◽  
Platelet Adhesion And Aggregation

scholarly journals Microfluidic chip grafted with integrin tension sensors for evaluating the effects of flowing shear stress and ROCK inhibitor on platelets

Lab on a Chip ◽  
2021 ◽  
Author(s):  
Subin Mao ◽  
Anwesha Sarkar ◽  
Yongliang Wang ◽  
Chao Song ◽  
Dana Nicole LeVine ◽  
...  
Keyword(s):  
Shear Stress ◽  
Microfluidic Chip ◽  
Platelet Adhesion ◽  
Rock Inhibitor ◽  
Platelet Adhesion And Aggregation ◽  
Key Players

Integrins are key players in platelet adhesion and aggregation. Integrin molecular tensions, the forces transmitted by integrin molecules, are regulated by both mechanical and biochemical cues, and the outside-in and...

scholarly journals Glycoprotein Ibα–Mediated Platelet Adhesion and Aggregation to Immobilized Thrombin Under Conditions of Flow

2006 ◽  
Vol 26 (3) ◽  
pp. 670-675 ◽  
Author(s):  
Cees Weeterings ◽  
Jelle Adelmeijer ◽  
Timothy Myles ◽  
Philip G. de Groot ◽  
Ton Lisman
Keyword(s):  
Platelet Adhesion ◽  
Platelet Adhesion And Aggregation

Simulation of platelet adhesion and aggregation regulated by fibrinogen and von Willebrand factor

2008 ◽  
Vol 99 (01) ◽  
pp. 108-115 ◽  
Author(s):  
Koichiro Yano ◽  
Ken-ichi Tsubota ◽  
Takuji Ishikawa ◽  
Shigeo Wada ◽  
Takami Yamaguchi ◽  
...  
Keyword(s):  
Platelet Adhesion ◽  
Thrombus Formation ◽  
Simple Shear Flow ◽  
Stokesian Dynamics ◽  
General Observation ◽  
Significant Development ◽  
Platelet Adhesion And Aggregation ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryWe propose a method to analyze platelet adhesion and aggregation computationally, taking into account the distinct properties of two plasma proteins, vonWillebrand factor (vWF) and fibrinogen (Fbg). In this method, the hydrodynamic interactions between platelet particles under simple shear flow were simulated using Stokesian dynamics based on the additivity of velocities. The binding force between particles mediated by vWF and Fbg was modeled using the Voigt model. Two Voigt models with different properties were introduced to consider the distinct behaviors of vWF and Fbg. Our results qualitatively agreed with the general observation of a previous in-vitro experiment, thus demonstrating that the significant development of thrombus formation in height requires not only vWF, but also Fbg. This agreement of simulation and experimental results qualitatively validates our model and suggests that consideration of the distinct roles of vWF and Fbg is essential to investigate the physiological and pathophysiological mechanisms of thrombus formation using a computational approach.

Regulation der primären Hämostase durch von-Willebrand-Faktor und ADAMTS13

2011 ◽  
Vol 31 (04) ◽  
pp. 275-280 ◽  
Author(s):  
U. Budde ◽  
R. Schneppenheim
Keyword(s):  
Platelet Adhesion ◽  
Coagulation Factor ◽  
Von Willebrand Disease ◽  
Coagulation Cascade ◽  
Platelet Glycoprotein ◽  
Platelet Adhesion And Aggregation ◽  
Hydrodynamic Shear ◽  
Specific Protease ◽  
Multiple Domains ◽  
Von Willebrand

SummaryVon Willebrand factor (VWF) is an adhesive, multi-functional huge multimerized protein with multiple domains harboring binding sites for collagen, platelet glycoprotein receptors and coagulation factor VIII (FVIII). The functional domains enable VWF to bind to the injured vessel wall, to recruit platelets to the site of injury by adhesion and aggregation and to bind and protect FVIII, an important cofactor of the coagulation cascade. VWF function in primary haemostasis is located in particular in the arterial and micro-circulation. This environment is exposed to high shear forces with hydrodynamic shear rates ranging over several orders of magnitude from 10–1 to 105 s-1 and requires particular mechanisms to enable platelet adhesion and aggregation under these variable conditions. The respective VWF function is strictly correlating with its multimer size. Lack or reduction of large VWF multimers is seen in patients with von Willebrand disease (VWD) type 2A which correlates with reduction of both VWF:platelet GPIb-binding and VWF:collagen binding and a bleeding phenotype. To prevent unlimited platelet adhesion and aggregation which is the cause of the microangiopathic disorder thrombotic thrombocytopenic purpura (TTP), VWF function is regulated by its specific protease ADAMTS13. Whereas a particular susceptibility of VWF to ADAMTS13 proteolysis is the cause of a frequent VWD type 2A phenotype, lack or dysfunction of ADAMTS13, either acquired by ADAMTS13 antibodies or by inherited ADAMTS13 deficiency (Upshaw-Schulman Syndrome), causes TTP. Therefore VWD and TTP represent the opposite manifestations of VWF related disorders, tightly linked to each other.

scholarly journals Platelet adhesion and aggregation on polyethylene: Effect of exhaustive exercise

2003 ◽  
Vol 68B (1) ◽  
pp. 53-58 ◽  
Author(s):  
Marco Bonifazi ◽  
Anna Maria Aloisi ◽  
Ilaria Ceccarelli ◽  
Stefania Lamponi ◽  
Leda Lodi ◽  
...  
Keyword(s):  
Platelet Adhesion ◽  
Exhaustive Exercise ◽  
Platelet Adhesion And Aggregation

Crystal structure of agkisacucetin, a Gpib-binding snake C-type lectin that inhibits platelet adhesion and aggregation

2012 ◽  
Vol 80 (6) ◽  
pp. 1707-1711 ◽  
Author(s):  
Yongxiang Gao ◽  
Honghua Ge ◽  
Hongkai Chen ◽  
Heng Li ◽  
Yiwei Liu ◽  
...  
Keyword(s):  
Crystal Structure ◽  
Platelet Adhesion ◽  
Platelet Adhesion And Aggregation

scholarly journals Platelet adhesion and aggregation on human type VI collagen surfaces under physiological flow conditions

Blood ◽  
1995 ◽  
Vol 85 (7) ◽  
pp. 1826-1835 ◽  
Author(s):  
JM Ross ◽  
LV McIntire ◽  
JL Moake ◽  
JH Rand
Keyword(s):  
Shear Rate ◽  
Platelet Adhesion ◽  
Surface Coverage ◽  
Wall Shear Rate ◽  
Flow Conditions ◽  
Collagen Vi ◽  
Type Vi Collagen ◽  
Platelet Adhesion And Aggregation ◽  
Von Willebrand ◽  
Low Shear

Type VI collagen is a subendothelial constituent that binds von Willebrand factor (vWF) and platelets. The interaction of platelets with type VI collagen and the roles of platelet glycoprotein (GP) receptors and vWF were studied under flow conditions using epi-fluorescent videomicroscopy coupled with digital image processing. We found that surface coverage was less than 6% on collagen VI at a relatively high-wall shear rate (1,000 s-1) and was approximately 60% at a low-wall shear rate (100 s-1). The molecular mechanisms involved in low-shear platelet binding were studied using monoclonal antibodies to platelet GPIb and GPIIb-IIIa, and polymeric aurin tricarboxylic acid. Anti-GPIIb-IIIa was the most effective in eliminating adhesion (surface coverage, 0.8%), followed by anti-GPIb (4.3%), and ATA (12.6%). Experiments with von Willebrand disease blood indicate that vWF is involved in platelet adhesion to collagen VI at 100 s-1. In the absence of vWF, there may be direct binding of platelet GPIIb-IIIa complexes to collagen VI. Adhesion and aggregation on collagen VI are different in shear rate dependence from collagen I. Our results suggest a possible role for collagen VI and vWF in platelet adhesion and aggregation in vascular regions with low shear rates.

Sign in / Sign up

Export Citation Format

Share Document