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Blood Cell Changes in Complement Activation-Related Pseudoallergy: Intertwining of Cellular and Humoral Interactions
Published in Raj Bawa, János Szebeni, Thomas J. Webster, Gerald F. Audette, Immune Aspects of Biopharmaceuticals and Nanomedicines, 2019
P-selectin is a well-known adhesive protein on platelets that binds to PSGL-1 on vascular endothelium and leukocytes as a consequence of platelet activation. It is stored in the alpha granules of platelets and becomes translocated to the surface membrane rapidly upon activation, therefore its expression is a classical marker of platelet activity. The molecular structure of P-selectin contains 9 C binding domains, one of which has been identified as a C3b binding site. Hence, when P selectin gets to the surface of platelets upon activation, a binding site for C3b gets exposed in order to clear the C3b generated during concurrent C activation. Interestingly, the pathway of platelet activation-related C activation turns from ClQ-mediated classical into alternative as the secretory products of a granules, C1 inhibitor and factor D—that cleaves factor B to its active form—starts to act [43, 46].
Surface Chemistry for Cell Capture in Microfluidic Systems
Published in Iniewski Krzysztof, Integrated Microsystems, 2017
ShuQi Wang, Feng Xu, Alexander Chi Fai Ip, Mrudula Somu, Xiaohu Zhao, Altug Akay, Utkan Demirci
The capture efficiency of a device is dependent on the number of capture moieties (e.g., antibodies and nucleic acids) on the surface. NPs can potentially improve cell capture efficiency by increasing the cell-capture surface area in a microchannel, thereby increasing the number of capture moieties. To do so, Han et al. [32] coated positively charged colloidal silica NPs (10–15 nm) onto the channel surface via negatively charged poly-L-lysine (PLL) (Figure 25.3). Using this strategy, up to 35% additional capture moieties (e.g., P-selectin) were obtained as compared to adsorption in the uncoated channel. In addition, Han and colleagues used titanium (IV) butoxide as an adhesive to coat NPs on the channel surface. The results showed that titanium (IV) butoxide had comparable capture efficiency as PLL. In both cases, the increased roughness on the channel surface and the increased number of the capturing moiety, P-selectin, significantly enhanced the rolling velocity of cells [32]. Enhanced cell rolling, due to the interaction between cells and P-selectin, can initiate cell adhesion on a target issue such as in the process of leukocyte homing and cancer cell metastasis [33]. As expected, the enhanced cell rolling significantly increased the cell capture efficiency [32]. However, it should be noted that the amount of coated NPs needs to be optimized. Otherwise, excessive NPs coated on the channel surface may aggregate and occlude the microchannel.
Targeted MRI
Published in Robert J. Gropler, David K. Glover, Albert J. Sinusas, Heinrich Taegtmeyer, Cardiovascular Molecular Imaging, 2007
Susan B. Yeon, Andrea J. Wiethoff, Warren J. Manning, Elmar Spuentrup, Rene M. Botnar
Vascular inflammation and associated endothelial activation is believed to play an integral role in initiation and progression of atherosclerosis. Endothelial activation is characterized by the upregulation of leukocyte adhesion molecules such as E- and P-selectin, which facilitate adhesion and migration of monocytes. Differentiation of monocytes into macrophages and subsequent digestion of lipoproteins by macrophages occur in a later stage and eventually lead to the accumulation of lipid filled macrophages, which are believed to be a precursor of rupture-prone vulnerable plaque.
Study of functional drug-eluting stent in promoting endothelialization and antiproliferation
Published in Journal of Biomaterials Science, Polymer Edition, 2020
Ruixia Hou, Leigang Wu, Yabin Zhu, Jin Wang, Zhilu Yang, Qiufen Tu, Nan Huang
P-selectin, also called GMP140, is a 140-kDa granule membrane protein which can be up-regulated by a factor of 10 on the surface membrane of platelets after activation [31]. Therefore, an assessment of P-selectin expression is one of the methods to show platelet activation. Based on fluorescence results (Figure 4(A)), compared with the SS and Ti-O surfaces, there was a lower amount of P-selectin on the P50 surface. For the P50T5, P50T20, and P50T42 samples, there was almost no P-selectin expression because of the inhibitory effect of tacrolimus, and there were almost no platelet clots. Platelet behavior was further evaluated using quantitative P-selectin (GMP140), LDH, and fibrinogen denaturation (γ-chain) assays (Figure 4(B)). These quantitative results demonstrated the same trend as the platelet adhesion and P-selectin staining images. Compared with the other samples, the most serious platelet activation was observed on the SS surface, and the Ti-O and P50 samples were better than the SS sample. After drug was loaded into P50, the GMP140, LDH, and γ-chain values were obviously lower on the P50T5, P50T20, and P50T42 surfaces than on the SS, Ti-O, and P50 surfaces. Higher drug content appeared to lead to the best inhibition. These results demonstrate that tacrolimus plays an important role in inhibiting platelet adhesion, and activation, and it can improve hemocompatibility.
Immobilizing argatroban and mPEG-NH2 on a polyethersulfone membrane surface to prepare an effective nonthrombogenic biointerface
Published in Journal of Biomaterials Science, Polymer Edition, 2019
Yanling Dai, Siyuan Dai, Xiaohui Xie, Jianping Ning
Platelets play an important role in thrombosis and are also vital in evaluating the blood compatibility. This is because the blood contacts the biomaterial surface and a layer of adsorbed protein forms first, followed by platelet adhesion [59]. Then, the platelets are activated via various stimuli that trigger complex pathways, dramatically changing the shape of the platelets, promoting aggregation with other platelets and the release of potent prothrombotic agonists [59]. P-selectin (CD62p), also known as platelet activation-dependent α-granule membrane protein 140, is employed to evaluate the degree of activation of platelets. CD41b, a transmembrane glycoprotein, combines with CD61 to form the GPIIb/IIIa (CD41b/CD61) complex, which relates to platelet activation, aggregation and adhesion. In this work, CD62p and CD41b were labeled with PE-CyTM5 mouse anti-human CD62p and FITC mouse anti-human CD41b, respectively, and the platelets adhered to and activated by the sample membranes were analyzed by immunofluorescence [46].
Platelet adhesion potential estimation in a normal and diseased coronary artery model: effects of shear stress magnitude versus shear stress history
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2022
The adhesion and thrombotic molecules of interest in this study are tissue factor, CD41a, CD42b and CD62P. Tissue factor is expressed on activated vascular cells and is a major regulator of the extrinsic coagulation pathway (Houston et al. 1999). CD41a (GPIIb) is necessary for platelet aggregation to fibrin and clot formation (Liu et al. 2009). CD42b (GPIba) interacts with von Willebrand factor and therefore plays a role in platelet adhesion (Fuchs et al. 2010). CD62P (P-selectin) is associated with platelet activation and plays a role in leukocyte recruitment and adhesion (Wein et al. 1995). Each of these molecules plays an important role in CHD development and progression.