Log in

Relevant bibliographies by topics / Adhesion of platelets / Journal articles

To see the other types of publications on this topic, follow the link: Adhesion of platelets.

Journal articles on the topic 'Adhesion of platelets'

Author: Grafiati

Published: 3 June 2025

Last updated: 1 August 2025

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Adhesion of platelets.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Adam, Frederic, Shilun Zheng, Aurelio V. Santos, John G. Kelton та Catherine P. M. Hayward. "Mechanisms of Static and Shear-Induced Platelet Adhesion: Differences in the Adhesion Supported by MMRN1 Comparisons with Other β3 Integrin Ligands." Blood 106, № 11 (2005): 2659. http://dx.doi.org/10.1182/blood.v106.11.2659.2659.

Full text

Abstract:

Abstract Platelet adhesion and aggregation at the site of vascular injury are key events in hemostasis and thrombosis. These processes are supported by interactions between platelet glycoprotein (GP) receptors (including integrin αIIbβ3, GP Ib-IX-V and GPVI) and ligands that include von Willebrand factor (VWF), collagen, and fibrinogen (Fg). Recently, the polymeric protein multimerin 1 (MMRN1) was identified to bind β3 integrins. Normally, MMRN1 is sequestered within secretion granules of platelets, megakaryocytes, and endothelium until its release. In static adhesion assays, MMRN1 supports pl

APA, Harvard, Vancouver, ISO, and other styles

2

Bombeli, Thomas, Barbara R. Schwartz та John M. Harlan. "Adhesion of Activated Platelets to Endothelial Cells: Evidence for a GPIIbIIIa-dependent Bridging Mechanism and Novel Roles for Endothelial Intercellular Adhesion Molecule 1 (ICAM-1), αvβ3 Integrin, and GPIbα". Journal of Experimental Medicine 187, № 3 (1998): 329–39. http://dx.doi.org/10.1084/jem.187.3.329.

Full text

Abstract:

Although it has been reported that activated platelets can adhere to intact endothelium, the receptors involved have not been fully characterized. Also, it is not clear whether activated platelets bind primarily to matrix proteins at sites of endothelial cell denudation or directly to endothelial cells. Thus, this study was designed to further clarify the mechanisms of activated platelet adhesion to endothelium. Unstimulated human umbilical vein endothelial cell (HUVEC) monolayers were incubated with washed, stained, and thrombin-activated human platelets. To exclude matrix involvement, HUVEC

APA, Harvard, Vancouver, ISO, and other styles

3

Canalli, Andreia A., Carla F. Franco-Penteado, Fabiola Traina, et al. "Altered Red Cell and Platelet Adhesion in the Hemolytic Diseases: Hereditary Spherocytosis, Paroxysmal Nocturnal Hemoglobinuria and Sickle Cell Anemia." Blood 108, no. 11 (2006): 1238. http://dx.doi.org/10.1182/blood.v108.11.1238.1238.

Full text

Abstract:

Abstract Increasing evidence exists to suggest that intravascular hemolysis may have important pathophysiological consequences resulting from reduced vascular nitric oxide (NO) bioavailability due to hemoglobin-mediated NO scavenging; such consequences may include endothelial dysfunction and vasculopathy. Hemolytic diseases such as hereditary spherocytosis (HS), paroxysmal nocturnal hemoglobinuria (PNH) and sickle cell anemia (SCA), despite having diverse etiologies, share a number of complications that include pulmonary and systolic arterial hypertension, cutaneous leg ulcerations and, in PNH

APA, Harvard, Vancouver, ISO, and other styles

4

Kuwahara, Mitsuhiro, Mitsuhiko Sugimoto, Shizuko Tsuji, Shigeki Miyata, and Akira Yoshioka. "Cytosolic Calcium Changes in a Process of Platelet Adhesion and Cohesion on a von Willebrand Factor-Coated Surface Under Flow Conditions." Blood 94, no. 4 (1999): 1149–55. http://dx.doi.org/10.1182/blood.v94.4.1149.

Full text

Abstract:

Abstract Recent flow studies indicated that platelets are transiently captured onto and then translocated along the surface through interaction of glycoprotein (GP) Ib with surface-immobilized von Willebrand factor (vWF). During translocation, platelets are assumed to be activated, thereafter becoming firmly adhered and cohered on the surface. In exploring the mechanisms by which platelets become activated during this process, we observed changes in platelet cytosolic calcium concentrations ([Ca2+]i) concomitantly with the real-time platelet adhesive and cohesive process on a vWF-coated surfac

APA, Harvard, Vancouver, ISO, and other styles

5

Kuwahara, Mitsuhiro, Mitsuhiko Sugimoto, Shizuko Tsuji, Shigeki Miyata, and Akira Yoshioka. "Cytosolic Calcium Changes in a Process of Platelet Adhesion and Cohesion on a von Willebrand Factor-Coated Surface Under Flow Conditions." Blood 94, no. 4 (1999): 1149–55. http://dx.doi.org/10.1182/blood.v94.4.1149.416k18_1149_1155.

Full text

Abstract:

Recent flow studies indicated that platelets are transiently captured onto and then translocated along the surface through interaction of glycoprotein (GP) Ib with surface-immobilized von Willebrand factor (vWF). During translocation, platelets are assumed to be activated, thereafter becoming firmly adhered and cohered on the surface. In exploring the mechanisms by which platelets become activated during this process, we observed changes in platelet cytosolic calcium concentrations ([Ca2+]i) concomitantly with the real-time platelet adhesive and cohesive process on a vWF-coated surface under f

APA, Harvard, Vancouver, ISO, and other styles

6

Yamanouchi, Jun, Jun An, Hiroshi Fujiwara, Yoshihiro Yakushijin, Takaaki Hato та Masaki Yasukawa. "Activation of Integrin αIIbβ3 through Toll-Like Receptors in Platelets." Blood 110, № 11 (2007): 3892. http://dx.doi.org/10.1182/blood.v110.11.3892.3892.

Full text

Abstract:

Abstract [Purpose] Toll-like receptors (TLRs) play a critical role in innate immunity by recognizing the great conserved structures on various bacteria, viruses, and fungi. Recently, several groups reported that TLRs are expressed in human platelets and that platelet TLR4 participates in the defense mechanism against bacteria. Although TLRs are known to activate intracellular signaling pathways leading to various immune responses, the platelet responses to TLR ligands are poorly characterized. In this study, we examined whether TLR lignads can induce activation of platelet major integrin, αllb

APA, Harvard, Vancouver, ISO, and other styles

7

Moroi, Masaaki, Stephanie M. Jung, Shosaku Nomura, Sadayoshi Sekiguchi, Antonio Ordinas, and Maribel Diaz-Ricart. "Analysis of the Involvement of the von Willebrand Factor–Glycoprotein Ib Interaction in Platelet Adhesion to a Collagen-Coated Surface Under Flow Conditions." Blood 90, no. 11 (1997): 4413–24. http://dx.doi.org/10.1182/blood.v90.11.4413.

Full text

Abstract:

Abstract The requisite initial reaction for in vivo thrombus formation in flowing blood is platelet adhesion to the exposed surface of the extracellular matrix. The contribution of von Willebrand factor (vWF ) in plasma and glycoprotein (GP) Ib on the platelet membrane to platelet adhesion has been well-documented. We have recently developed a procedure (the “flow adhesion assay”) for measuring platelet adhesion under flow conditions that allowed us to characterize platelet adhesion to a collagen-coated surface. Here, we apply our method to analyze platelet adhesion to a vWF-coated surface to

APA, Harvard, Vancouver, ISO, and other styles

8

Moroi, Masaaki, Stephanie M. Jung, Shosaku Nomura, Sadayoshi Sekiguchi, Antonio Ordinas, and Maribel Diaz-Ricart. "Analysis of the Involvement of the von Willebrand Factor–Glycoprotein Ib Interaction in Platelet Adhesion to a Collagen-Coated Surface Under Flow Conditions." Blood 90, no. 11 (1997): 4413–24. http://dx.doi.org/10.1182/blood.v90.11.4413.4413_4413_4424.

Full text

Abstract:

The requisite initial reaction for in vivo thrombus formation in flowing blood is platelet adhesion to the exposed surface of the extracellular matrix. The contribution of von Willebrand factor (vWF ) in plasma and glycoprotein (GP) Ib on the platelet membrane to platelet adhesion has been well-documented. We have recently developed a procedure (the “flow adhesion assay”) for measuring platelet adhesion under flow conditions that allowed us to characterize platelet adhesion to a collagen-coated surface. Here, we apply our method to analyze platelet adhesion to a vWF-coated surface to determine

APA, Harvard, Vancouver, ISO, and other styles

9

Zijenah, L. S., L. F. Morton, and M. J. Barnes. "Platelet adhesion to collagen. Factors affecting Mg2+-dependent and bivalent-cation-independent adhesion." Biochemical Journal 268, no. 2 (1990): 481–86. http://dx.doi.org/10.1042/bj2680481.

Full text

Abstract:

Platelet adhesion to collagens immobilized on plastic has been measured, with the following results. (1) Human, but not rabbit, platelets adhered readily to pepsin-extracted monomeric collagens in an Mg2(+)-dependent manner. (2) Rabbit platelets adhered to a monomeric collagen extracted without pepsin by a process that was cation-independent; human platelet adhesion to this collagen exhibited a cation-independent element. (3) Human platelet adhesion to polymeric collagens, including intact native fibres and those reconstituted from pepsin-extracted monomeric collagens, exhibited appreciable ca

APA, Harvard, Vancouver, ISO, and other styles

10

Walker, Britta, Syeda T. Towhid, Evi Schmid, et al. "Dynamic adhesion of eryptotic erythrocytes to immobilized platelets via platelet phosphatidylserine receptors." American Journal of Physiology-Cell Physiology 306, no. 3 (2014): C291—C297. http://dx.doi.org/10.1152/ajpcell.00318.2013.

Full text

Abstract:

Glucose depletion of erythrocytes triggers suicidal erythrocyte death or eryptosis, which leads to cell membrane scrambling with phosphatidylserine exposure at the cell surface. Eryptotic erythrocytes adhere to endothelial cells by a mechanism involving phosphatidylserine at the erythrocyte surface and CXCL16 as well as CD36 at the endothelial cell membrane. Nothing has hitherto been known about an interaction between eryptotic erythrocytes and platelets, the decisive cells in primary hemostasis and major players in thrombotic vascular occlusion. The present study thus explored whether and how

APA, Harvard, Vancouver, ISO, and other styles

11

Saelman, EU, B. Kehrel, KM Hese, PG de Groot, JJ Sixma, and HK Nieuwenhuis. "Platelet adhesion to collagen and endothelial cell matrix under flow conditions is not dependent on platelet glycoprotein IV." Blood 83, no. 11 (1994): 3240–44. http://dx.doi.org/10.1182/blood.v83.11.3240.3240.

Full text

Abstract:

Abstract Platelet membrane glycoprotein IV (GPIV) is a cell-surface glycoprotein that has been proposed as a receptor for collagen. Recently, it has been shown that platelets with the Naka-negative phenotype lack GPIV on their surface, whereas donors with this phenotype are healthy and do not suffer from hematologic disorders. In this study, we compared Naka- negative platelets with normal platelets in adhesion to collagen types I, III, IV, and V and the extracellular matrix of endothelial cells (ECM) under static and flow conditions. No differences in platelet adhesion and subsequent aggregat

APA, Harvard, Vancouver, ISO, and other styles

12

Saelman, EU, B. Kehrel, KM Hese, PG de Groot, JJ Sixma, and HK Nieuwenhuis. "Platelet adhesion to collagen and endothelial cell matrix under flow conditions is not dependent on platelet glycoprotein IV." Blood 83, no. 11 (1994): 3240–44. http://dx.doi.org/10.1182/blood.v83.11.3240.bloodjournal83113240.

Full text

Abstract:

Platelet membrane glycoprotein IV (GPIV) is a cell-surface glycoprotein that has been proposed as a receptor for collagen. Recently, it has been shown that platelets with the Naka-negative phenotype lack GPIV on their surface, whereas donors with this phenotype are healthy and do not suffer from hematologic disorders. In this study, we compared Naka- negative platelets with normal platelets in adhesion to collagen types I, III, IV, and V and the extracellular matrix of endothelial cells (ECM) under static and flow conditions. No differences in platelet adhesion and subsequent aggregate formati

APA, Harvard, Vancouver, ISO, and other styles

13

Ilton, Marcus K., Marcia L. Taylor, Neil L. A. Misso, Philip J. Thompson, and Joseph Hung. "Neutrophil Cathepsin G Modulates Platelet P-Selectin Expression and Inhibits P-Selectin-Mediated Platelet-Neutrophil Adhesion." Clinical Science 94, no. 4 (1998): 437–45. http://dx.doi.org/10.1042/cs0940437.

Full text

Abstract:

1. Close contact between platelets and neutrophils modulates their cellular interactions in thrombotic and inflammatory states, with stimulation of P-selectin expression on platelets by agonists such as thrombin and neutrophil-derived cathepsin G being critical in mediating platelet—neutrophil adhesion. This study compared the effects of thrombin and cathepsin G on platelet P-selectin expression and on P-selectin-mediated platelet—neutrophil adhesion. 2. Washed platelets and platelet—neutrophil mixed cell suspensions (platelet/neutrophil ratio, 10:1) were incubated with either the supernatant

APA, Harvard, Vancouver, ISO, and other styles

14

Kulkarni, Suhasini, Kevin J. Woollard, Stephen Thomas, David Oxley, and Shaun P. Jackson. "Conversion of platelets from a proaggregatory to a proinflammatory adhesive phenotype: role of PAF in spatially regulating neutrophil adhesion and spreading." Blood 110, no. 6 (2007): 1879–86. http://dx.doi.org/10.1182/blood-2006-08-040980.

Full text

Abstract:

Abstract The ability of platelets to provide a highly reactive surface for the recruitment of other platelets and leukocytes to sites of vascular injury is critical for hemostasis, atherothrombosis, and a variety of inflammatory diseases. The mechanisms coordinating platelet-platelet and platelet-leukocyte interactions have been well defined and, in general, it is assumed that increased platelet activation correlates with enhanced reactivity toward other platelets and neutrophils. In the current study, we demonstrate a differential role for platelets in supporting platelet and neutrophil adhes

APA, Harvard, Vancouver, ISO, and other styles

15

Ostrovsky, Lena, Alison J. King, Samantha Bond, et al. "A Juxtacrine Mechanism for Neutrophil Adhesion on Platelets Involves Platelet-Activating Factor and a Selectin-Dependent Activation Process." Blood 91, no. 8 (1998): 3028–36. http://dx.doi.org/10.1182/blood.v91.8.3028.3028_3028_3036.

Full text

Abstract:

The aim of this study was to identify the molecular mechanisms involved in neutrophil adhesion to immobilized platelets with particular focus on the possible existence of a juxtacrine system for neutrophil-platelet interactions. Platelets were immobilized onto collagen (type I)-coated coverslips that were placed in a flow chamber and neutrophils were perfused across these confluent monolayers at a shear stress of 1 to 4 dynes/cm2. Neutrophils rolled, and a significant proportion (25% to 50%) adhered to platelet monolayers. P-selectin was expressed in very large quantities on the surface of pla

APA, Harvard, Vancouver, ISO, and other styles

16

Urieli-Shoval, Simcha, George Shubinsky, Reinhold P. Linke, Mati Fridkin, Israel Tabi, and Yaacov Matzner. "Adhesion of human platelets to serum amyloid A." Blood 99, no. 4 (2002): 1224–29. http://dx.doi.org/10.1182/blood.v99.4.1224.

Full text

Abstract:

Serum amyloid A (SAA) is an acute phase reactant, and its level in the blood is elevated to 1000-fold in response of the body to trauma, infection, inflammation, and neoplasia. SAA was reported to inhibit platelet aggregation and to induce adhesion of leukocytes. This study looked at adhesion of human platelets to SAA. Immobilized SAA supported the adhesion of human washed platelets; level of adhesion to SAA was comparable to fibronectin and lower than to fibrinogen. Adhesion to SAA was further enhanced by Mn2+ and the physiological agonist, thrombin. Platelet adhesion to SAA was completely ab

APA, Harvard, Vancouver, ISO, and other styles

17

Watts, Tim, Mostafa Barigou, and Gerard B. Nash. "Comparative rheology of the adhesion of platelets and leukocytes from flowing blood: why are platelets so small?" American Journal of Physiology-Heart and Circulatory Physiology 304, no. 11 (2013): H1483—H1494. http://dx.doi.org/10.1152/ajpheart.00881.2012.

Full text

Abstract:

We investigated rheological adaptation of leukocytes and platelets for their adhesive functions in inflammation and hemostasis, respectively. Adhesion and margination of leukocytes or platelets were quantified for blood perfused through capillaries coated with P-selectin or collagen, when flow rate, suspending phase viscosity, red cell aggregation, or rigidity was modified. Independent variation of shear rate and shear stress indicated that the ability of platelets to attach at higher levels than leukocytes was largely attributable to their smaller size, reducing their velocity before attachme

APA, Harvard, Vancouver, ISO, and other styles

18

Polanowska-Grabowska, R., M. Geanacopoulos та A. R. L. Gear. "Platelet adhesion to collagen via the α2β1 integrin under arterial flow conditions causes rapid tyrosine phosphorylation of pp125FAK". Biochemical Journal 296, № 3 (1993): 543–47. http://dx.doi.org/10.1042/bj2960543.

Full text

Abstract:

Adhesion of human platelets to collagen under arterial flow conditions mediated by the alpha 2 beta 1 integrin increased tyrosine phosphorylation of several proteins, one of which was the focal adhesion tyrosine kinase, pp125FAK. Tyrosine phosphorylation of pp125FAK did not occur in non-adherent flowing platelets or in platelets attached to poly(L-lysine). Neither adhesion nor tyrosine phosphorylation was affected by pretreatment of platelets with GRGDSP peptide or by anti-alpha IIb beta 3 monoclonal antibody P2. Adherent platelets retained their discoid shape, suggesting that induction of pp1

APA, Harvard, Vancouver, ISO, and other styles

19

Przygodzki, Tomasz, Boguslawa Luzak, Hassan Kassassir, et al. "Diabetes and Hyperglycemia Affect Platelet GPIIIa Expression: Effects on Adhesion Potential of Blood Platelets from Diabetic Patients under In Vitro Flow Conditions." International Journal of Molecular Sciences 21, no. 9 (2020): 3222. http://dx.doi.org/10.3390/ijms21093222.

Full text

Abstract:

Blood platelets play a crucial role in the early stages of atherosclerosis development. The process is believed to require firm adhesion of platelets to atherosclerosis-prone sites of the artery. However, little evidence exists regarding whether the blood platelets of individuals with pathological conditions associated with atherosclerosis have higher potential for adhesion. This process is to a large extent dependent on receptors present on the platelet membrane. Therefore, the aim of the presented study was to determine whether blood platelets from diabetic patients have higher capacity of a

APA, Harvard, Vancouver, ISO, and other styles

20

Ju, Lining, Cheng Zhu, Miguel A. Cruz, and Yunfeng Chen. "The Study of GPIb-VWF Mediated Early-Stage Platelet Activation Triggering On a Single Cell." Blood 120, no. 21 (2012): 1069. http://dx.doi.org/10.1182/blood.v120.21.1069.1069.

Full text

Abstract:

Abstract Abstract 1069 Binding of GPIbα to VWF tethers platelets to disrupted vascular surface during the haemostatic process. The GPIbα –VWF interaction can also trigger outside-in signaling cascade, resulting in platelet activation, characterized by morphological transformation from discoid to a more spiky shape as well as activation of integrin α IIbβ3. Using the adhesion frequency assay with a biomembrane force probe (BFP), we studied signal initiation by repeated brief contacts of a single platelet with a glass bead coated with VWF-A1 domain and/or fibronectin III 7–10 domain (FNIII7–10)

APA, Harvard, Vancouver, ISO, and other styles

21

Lahav, Judith, Eveline M. Wijnen, Oded Hess та ін. "Enzymatically catalyzed disulfide exchange is required for platelet adhesion to collagen via integrin α2β1". Blood 102, № 6 (2003): 2085–92. http://dx.doi.org/10.1182/blood-2002-06-1646.

Full text

Abstract:

Abstract Integrin α2β1 is the principal adhesive receptor for collagen but platelets also adhere through glycoprotein VI (GPVI). Integrin αIIbβ3 may augment platelet adhesion. We have shown that disulfide exchange is necessary for platelet adhesion to fibrinogen, fibronectin, and collagen. However 2 questions remained: (1) Can activated αIIbβ3 explain the observed role of disulfide exchange in adhesion to collagen, or is this role common to other integrins? (2) Is disulfide dependence specific to the integrin receptors or shared with GPVI? To discriminate adhesive functions of α2β1 from those

APA, Harvard, Vancouver, ISO, and other styles

22

Zaidi, TN, LV McIntire, DH Farrell, and P. Thiagarajan. "Adhesion of platelets to surface-bound fibrinogen under flow." Blood 88, no. 8 (1996): 2967–72. http://dx.doi.org/10.1182/blood.v88.8.2967.bloodjournal8882967.

Full text

Abstract:

After platelet activation, fibrinogen mediates platelet-platelet interactions leading to platelet aggregation. In addition, fibrinogen can also function as a cell adhesion molecule, providing a substratum for adhesion of platelets and endothelial cells. In this report, we studied the adhesion of platelets to surface-immobilized fibrinogen under flow in different shear rates. Heparinized whole blood containing mepacrine-labeled platelets was perfused for two minutes at various wall shear rates from 250 to 2,000 s-1 in a parallel plate flow chamber. The number of adherent fluorescent platelets w

APA, Harvard, Vancouver, ISO, and other styles

23

Shattil, Sanford. "Signaling Through Platelet Integrin αIIbβ3: Inside-out, Outside-in, and Sideways". Thrombosis and Haemostasis 82, № 08 (1999): 318–25. http://dx.doi.org/10.1055/s-0037-1615849.

Full text

Abstract:

IntroductionCell adhesion, which plays a major role in the response of tissues to injury, involves a wide variety of cells, adhesion receptors, and ligands. Prominent among the cells responding to injury are platelets, the first line of defense against hemorrhage and an early player in the overall process of wound-healing.1 Prominent among the adhesion receptors is αIIbβ3, a platelet-specific integrin essential for hemostasis by virtue of its role in mediating platelet aggregation and platelet spreading on vascular matrices. Prominent among the ligands for αIIbβ3 are the multivalent adhesive p

APA, Harvard, Vancouver, ISO, and other styles

24

McCarty, Owen J. T., Shaker A. Mousa, Paul F. Bray, and Konstantinos Konstantopoulos. "Immobilized platelets support human colon carcinoma cell tethering, rolling, and firm adhesion under dynamic flow conditions." Blood 96, no. 5 (2000): 1789–97. http://dx.doi.org/10.1182/blood.v96.5.1789.

Full text

Abstract:

Abstract Accumulating evidence suggests that successful metastatic spread may depend on the ability of tumor cells to undergo extensive interactions with platelets. However, the mechanisms mediating tumor cell adhesion to platelets under conditions of flow remain largely unknown. Therefore, this study was designed to analyze the ability of 3 human colon carcinoma cell lines (LS174T, COLO205, and HCT-8) to bind to surface-anchored platelets under flow and to identify the receptors involved in these processes. Immobilized platelets support LS174T cell adhesion at wall shear stresses up to 1.4 dy

APA, Harvard, Vancouver, ISO, and other styles

25

McCarty, Owen J. T., Shaker A. Mousa, Paul F. Bray, and Konstantinos Konstantopoulos. "Immobilized platelets support human colon carcinoma cell tethering, rolling, and firm adhesion under dynamic flow conditions." Blood 96, no. 5 (2000): 1789–97. http://dx.doi.org/10.1182/blood.v96.5.1789.h8001789_1789_1797.

Full text

Abstract:

Accumulating evidence suggests that successful metastatic spread may depend on the ability of tumor cells to undergo extensive interactions with platelets. However, the mechanisms mediating tumor cell adhesion to platelets under conditions of flow remain largely unknown. Therefore, this study was designed to analyze the ability of 3 human colon carcinoma cell lines (LS174T, COLO205, and HCT-8) to bind to surface-anchored platelets under flow and to identify the receptors involved in these processes. Immobilized platelets support LS174T cell adhesion at wall shear stresses up to 1.4 dyn/cm2. Ou

APA, Harvard, Vancouver, ISO, and other styles

26

Verheul, Henk M. W., Anita S. Jorna, Klaas Hoekman, Henk J. Broxterman, Martijn F. B. G. Gebbink, and Herbert M. Pinedo. "Vascular endothelial growth factor–stimulated endothelial cells promote adhesion and activation of platelets." Blood 96, no. 13 (2000): 4216–21. http://dx.doi.org/10.1182/blood.v96.13.4216.

Full text

Abstract:

Abstract Coagulation abnormalities, including an increased platelet turnover, are frequently found in patients with cancer. Because platelets secrete angiogenic factors on activation, this study tested the hypothesis that platelets contribute to angiogenesis. Stimulation with vascular endothelial growth factor (VEGF, 25 ng/mL) of human umbilical vein endothelial cells (HUVECs) promoted adhesion of nonactivated platelets 2.5-fold. In contrast, stimulation of HUVECs with basic fibroblast growth factor (bFGF) did not promote platelet adhesion. By blocking tissue factor (TF) activity, platelet adh

APA, Harvard, Vancouver, ISO, and other styles

27

Verheul, Henk M. W., Anita S. Jorna, Klaas Hoekman, Henk J. Broxterman, Martijn F. B. G. Gebbink, and Herbert M. Pinedo. "Vascular endothelial growth factor–stimulated endothelial cells promote adhesion and activation of platelets." Blood 96, no. 13 (2000): 4216–21. http://dx.doi.org/10.1182/blood.v96.13.4216.h8004216_4216_4221.

Full text

Abstract:

Coagulation abnormalities, including an increased platelet turnover, are frequently found in patients with cancer. Because platelets secrete angiogenic factors on activation, this study tested the hypothesis that platelets contribute to angiogenesis. Stimulation with vascular endothelial growth factor (VEGF, 25 ng/mL) of human umbilical vein endothelial cells (HUVECs) promoted adhesion of nonactivated platelets 2.5-fold. In contrast, stimulation of HUVECs with basic fibroblast growth factor (bFGF) did not promote platelet adhesion. By blocking tissue factor (TF) activity, platelet adhesion was

APA, Harvard, Vancouver, ISO, and other styles

28

Babinska, Anna, Tahir Ahmed, Olcay Batuman, et al. "F11-Receptor (F11R/JAM) Mediates Platelet Adhesion to Endothelial Cells: Role in Inflammatory Thrombosis." Thrombosis and Haemostasis 88, no. 11 (2002): 843–50. http://dx.doi.org/10.1055/s-0037-1613312.

Full text

Abstract:

SummaryThe F11 receptor (F11R) is a cell adhesion molecule (CAM), member of the immunoglobulin superfamily found on the surface of human platelets, and determined to play a role in platelet aggregation, secretion, adhesion and spreading. The same molecule is present also at tight junctions of endothelial cells (EC) where it is known as JAM and acts as a CAM through homophilic interactions. The role of F11R/JAM in the interaction of platelets with endothelial cells was investigated in the current studies. We report here that washed human platelets adhere specifically to a matrix made of immobil

APA, Harvard, Vancouver, ISO, and other styles

29

Langer, Harald, Andreas E. May, Andreas Bültmann, and Meinrad Gawaz. "ADAM15 is an adhesion receptor for platelet GPIIb-IIIa and induces platelet activation." Thrombosis and Haemostasis 94, no. 09 (2005): 555–61. http://dx.doi.org/10.1160/th04-12-0784.

Full text

Abstract:

SummaryCell adhesion and proteolytic matrix degradation are central processes in atherosclerosis. Being a member of the family of ADAMs (“a disintegrin and metalloproteinase”), metargidin (ADAM15) combines a metalloproteinase domain and an RGD aminoacid sequence. We studied the potential role of ADAM15 as an adhesion receptor on endothelial cells and interactions between platelets and ADAM15 with respect to platelet adhesion, activation and thrombus formation. ADAM15 was found to be expressed on cultured endothelial cells (HUVEC). Platelet adhesion to immobilized recombinantADAM15 was effectiv

APA, Harvard, Vancouver, ISO, and other styles

30

Rinder, HM, JL Bonan, CS Rinder, KA Ault, and BR Smith. "Activated and unactivated platelet adhesion to monocytes and neutrophils." Blood 78, no. 7 (1991): 1760–69. http://dx.doi.org/10.1182/blood.v78.7.1760.1760.

Full text

Abstract:

Abstract To examine the possible receptor-ligand pairs mediating adhesion of activated and “unactivated” platelets to leukocytes and the kinetics of leukocyte-platelet binding, we developed a flow cytometric assay using isolated cell fractions to accurately measure heterotypic cell adhesion, including both total leukocyte-platelet conjugate formation as well as the number of platelets bound per leukocyte. We have shown that (1) activated platelet binding to both polymorphonuclear leukocytes (PMN) and monocytes is dependent on both a specific epitope (blocked by monoclonal antibody G1) of granu

APA, Harvard, Vancouver, ISO, and other styles

31

Rinder, HM, JL Bonan, CS Rinder, KA Ault, and BR Smith. "Activated and unactivated platelet adhesion to monocytes and neutrophils." Blood 78, no. 7 (1991): 1760–69. http://dx.doi.org/10.1182/blood.v78.7.1760.bloodjournal7871760.

Full text

Abstract:

To examine the possible receptor-ligand pairs mediating adhesion of activated and “unactivated” platelets to leukocytes and the kinetics of leukocyte-platelet binding, we developed a flow cytometric assay using isolated cell fractions to accurately measure heterotypic cell adhesion, including both total leukocyte-platelet conjugate formation as well as the number of platelets bound per leukocyte. We have shown that (1) activated platelet binding to both polymorphonuclear leukocytes (PMN) and monocytes is dependent on both a specific epitope (blocked by monoclonal antibody G1) of granule membra

APA, Harvard, Vancouver, ISO, and other styles

32

Fauvel-Lafeve, F., V. Tabaka, JP Caen, and YJ Legrand. "Defective adhesion of blood platelets to vascular microfibrils in the Bernard-Soulier syndrome." Blood 82, no. 7 (1993): 1985–88. http://dx.doi.org/10.1182/blood.v82.7.1985.1985.

Full text

Abstract:

Abstract Bernard-Soulier syndrome (BSS) platelets, which lack the membrane glycoprotein complex Ib-IX, do not adhere to subendothelium. The adhesion of platelets from two patients with BSS to subendothelial microfibrils (MFs) and type I collagen was compared in an in vitro assay adapted to patients with low platelet count. With both patients, platelet adhesion to MFs was strongly defective, whereas the adhesion to collagen was normal. The involvement of GPIb in the MFs-induced platelet adhesion was confirmed by the inhibitory effect of a MoAb (AN51) to the von Willebrand (vWF) factor binding d

APA, Harvard, Vancouver, ISO, and other styles

33

Fauvel-Lafeve, F., V. Tabaka, JP Caen, and YJ Legrand. "Defective adhesion of blood platelets to vascular microfibrils in the Bernard-Soulier syndrome." Blood 82, no. 7 (1993): 1985–88. http://dx.doi.org/10.1182/blood.v82.7.1985.bloodjournal8271985.

Full text

Abstract:

Bernard-Soulier syndrome (BSS) platelets, which lack the membrane glycoprotein complex Ib-IX, do not adhere to subendothelium. The adhesion of platelets from two patients with BSS to subendothelial microfibrils (MFs) and type I collagen was compared in an in vitro assay adapted to patients with low platelet count. With both patients, platelet adhesion to MFs was strongly defective, whereas the adhesion to collagen was normal. The involvement of GPIb in the MFs-induced platelet adhesion was confirmed by the inhibitory effect of a MoAb (AN51) to the von Willebrand (vWF) factor binding domain of

APA, Harvard, Vancouver, ISO, and other styles

34

Massberg, Steffen, Georg Enders, Francine Cláudia de Melo Matos, et al. "Fibrinogen Deposition at the Postischemic Vessel Wall Promotes Platelet Adhesion During Ischemia-Reperfusion In Vivo." Blood 94, no. 11 (1999): 3829–38. http://dx.doi.org/10.1182/blood.v94.11.3829.

Full text

Abstract:

Abstract Following ischemia-reperfusion (I/R), platelet adhesion is thought to represent the initial event leading to remodeling and reocclusion of the vasculature. The mechanisms underlying platelet adhesion to the endothelium have not been completely established. Endothelial cells rendered ischemic acquire a procoagulant phenotype, characterized by fibrinogen accumulation. Therefore, we evaluated whether fibrinogen deposition during I/R mediates platelet adhesion. Using fluorescence microscopy, fibrinogen deposition and the accumulation of platelets were assessed in vivo in a model of intest

APA, Harvard, Vancouver, ISO, and other styles

35

Massberg, Steffen, Georg Enders, Francine Cláudia de Melo Matos, et al. "Fibrinogen Deposition at the Postischemic Vessel Wall Promotes Platelet Adhesion During Ischemia-Reperfusion In Vivo." Blood 94, no. 11 (1999): 3829–38. http://dx.doi.org/10.1182/blood.v94.11.3829.423k35_3829_3838.

Full text

Abstract:

Following ischemia-reperfusion (I/R), platelet adhesion is thought to represent the initial event leading to remodeling and reocclusion of the vasculature. The mechanisms underlying platelet adhesion to the endothelium have not been completely established. Endothelial cells rendered ischemic acquire a procoagulant phenotype, characterized by fibrinogen accumulation. Therefore, we evaluated whether fibrinogen deposition during I/R mediates platelet adhesion. Using fluorescence microscopy, fibrinogen deposition and the accumulation of platelets were assessed in vivo in a model of intestinal I/R

APA, Harvard, Vancouver, ISO, and other styles

36

Krishnamurthi, S., and V. V. Kakkar. "Studies on the Effect of Platelet Inhibitors on Platelet Adhesion to Collagen and Collagen-Induced Human Platelet Activation." Thrombosis and Haemostasis 53, no. 03 (1985): 337–42. http://dx.doi.org/10.1055/s-0038-1661310.

Full text

Abstract:

SummaryThe effect of pyridoxal 5’-phosphate (PALP) and trifluoperazine (TFPZ), the calmodulin antagonist, on in vitro platelet adhesion to collagen and collagen-induced platelet activation was studied using platelet-rich-plasma (PRP) or washed platelets (WPL). Platelet aggregation and [14C]-5HT release induced by “threshold” or low concentrations of collagen (0.6 μg/ ml) in PRP were completely abolished by PALP (24 mM), TFPZ (250 μM) as well as indomethacin (10 μM). At higher concentrations of collagen (10–15 μg/ml) in PRP and WPL, the use of stirred and unstirred platelets treated with collag

APA, Harvard, Vancouver, ISO, and other styles

37

Cooper, Dianne, Keith D. Chitman, Matthew C. Williams, and D. Neil Granger. "Time-dependent platelet-vessel wall interactions induced by intestinal ischemia-reperfusion." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 6 (2003): G1027—G1033. http://dx.doi.org/10.1152/ajpgi.00457.2002.

Full text

Abstract:

Platelets roll and adhere in venules exposed to ischemia-reperfusion (I/R). This platelet-endothelial adhesion may influence leukocyte trafficking because platelet depletion decreases I/R-induced leukocyte emigration. The objectives of this study were 1) to assess the time course of platelet adhesion in the small bowel after I/R and 2) to determine the roles of endothelial and/or platelet P-selectin and P-selectin glycoprotein ligand-1 (PSGL-1) in this adhesion. The adhesion of fluorescently labeled platelets was monitored by intravital microscopy in postcapillary venules exposed to 45 min of

APA, Harvard, Vancouver, ISO, and other styles

38

Cooper, Dianne, Janice Russell, Keith D. Chitman, Matthew C. Williams, Robert E. Wolf, and D. Neil Granger. "Leukocyte dependence of platelet adhesion in postcapillary venules." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 5 (2004): H1895—H1900. http://dx.doi.org/10.1152/ajpheart.01000.2003.

Full text

Abstract:

Reperfusion of ischemic tissues results in development of a proinflammatory, prothrombogenic phenotype, culminating in the recruitment of leukocytes and platelets within postcapillary venules. Recent studies have indicated an interdependence of platelet and leukocyte adhesion, suggesting that heterotypic blood cell interactions may account for postischemic platelet recruitment. The objectives of this study were to 1) determine whether ischemia-reperfusion (I/R)-induced platelet recruitment is leukocyte dependent and 2) quantify the contributions of leukocytes and endothelial cells in this plat

APA, Harvard, Vancouver, ISO, and other styles

39

Morley, D. J., and I. A. Feuerstein. "Adhesion of Polymorphonuclear Leukocytes to Protein-Coated and Platelet Adherent Surfaces." Thrombosis and Haemostasis 62, no. 03 (1989): 1023–28. http://dx.doi.org/10.1055/s-0038-1651046.

Full text

Abstract:

SummarySince protein adsorption and platelet adhesion are likely to precede significant contact of leukocytes with the surfaces of artificial organs, we have chosen to study polymorphonuclear leukocyte (PMN) adhesion in a sequential manner. The work presented here deals with the effects of flow and surface type on PMN adhesion to fibrinogen- and albumin-coated glass. We compared direct adhesion to adsorbed protein with adhesion to adsorbed protein having adherent platelets. These experiments were designed to see if PMN's might preferentially adhere to albumin or fibrinogen and whether a partic

APA, Harvard, Vancouver, ISO, and other styles

40

Spangenberg, Peter, Helge Redlich, Iris Bergmann, Wolfgang Lösche, Matthias Götzrath, and Beate Kehrel. "The Platelet Glycoprotein IIb/IIIa Complex Is lnvolved in the Adhesion of Activated Platelets to Leukocytes." Thrombosis and Haemostasis 70, no. 03 (1993): 514–21. http://dx.doi.org/10.1055/s-0038-1649615.

Full text

Abstract:

SummaryThe adhesion of activated platelets to leukocytes (rosette formation) seems to be mediated by CD62 on platelets and its counterreceptor (CD 15 or a sialic acid-containing glycoprotein) on polymorphonuclear leukocytes (PMNL). However, neither treatment of platelets with an anti-CD62 antibody or fucoidan nor treatment of PMNL with anti-CD15 antibody or neuraminidase are able to inhibit completely the adhesion. Therefore, we have studied the platelet GPIIb/IIIa complex (CD41a) for its involvement in the adhesion of activated platelets to PMNL. The following evidences point to a participati

APA, Harvard, Vancouver, ISO, and other styles

41

Y. Pollitt, Alice, Kate Lowe, Arusa Latif, Gerard B. Nash, Steve P. Watson, and Leyre Navarro-Núñez. "Platelet adhesion to podoplanin under flow is mediated by the receptor CLEC-2 and stabilised by Src/Syk-dependent platelet signalling." Thrombosis and Haemostasis 113, no. 05 (2015): 1109–20. http://dx.doi.org/10.1160/th14-09-0762.

Full text

Abstract:

SummaryPlatelet-specific deletion of CLEC-2, which signals through Src and Syk kinases, or global deletion of its ligand podoplanin results in bloodfilled lymphatics during mouse development. Platelet-specific Syk deficiency phenocopies this defect, indicating that platelet activation is required for lymphatic development. In the present study, we investigated whether CLEC-2-podoplanin interactions could support platelet arrest from blood flow and whether platelet signalling is required for stable platelet adhesion to lymphatic endothelial cells (LECs) and recombinant podoplanin under flow. Pe

APA, Harvard, Vancouver, ISO, and other styles

42

Jandak, J., M. Steiner, and PD Richardson. "Alpha-tocopherol, an effective inhibitor of platelet adhesion." Blood 73, no. 1 (1989): 141–49. http://dx.doi.org/10.1182/blood.v73.1.141.141.

Full text

Abstract:

Abstract Platelet adhesiveness was tested ex vivo in a group of six normal individuals receiving varying doses of alpha-tocopherol. Adhesion to glass slides coated with fibronectin, collagen, fibrinogen, or plasma proteins was studied by perfusing platelet-rich plasma through a flow chamber that allowed time- and space-resolved observations of platelet adhesion. Platelet adherence was measured in an area of parallel flow lines and low shear rate under standardized conditions before and after dietary supplementation with vitamin E at doses of 200 and 400 IU/d. Platelet adherence differed in mag

APA, Harvard, Vancouver, ISO, and other styles

43

Jandak, J., M. Steiner, and PD Richardson. "Alpha-tocopherol, an effective inhibitor of platelet adhesion." Blood 73, no. 1 (1989): 141–49. http://dx.doi.org/10.1182/blood.v73.1.141.bloodjournal731141.

Full text

Abstract:

Platelet adhesiveness was tested ex vivo in a group of six normal individuals receiving varying doses of alpha-tocopherol. Adhesion to glass slides coated with fibronectin, collagen, fibrinogen, or plasma proteins was studied by perfusing platelet-rich plasma through a flow chamber that allowed time- and space-resolved observations of platelet adhesion. Platelet adherence was measured in an area of parallel flow lines and low shear rate under standardized conditions before and after dietary supplementation with vitamin E at doses of 200 and 400 IU/d. Platelet adherence differed in magnitude de

APA, Harvard, Vancouver, ISO, and other styles

44

Lalor, Patricia F., John Herbert, Roy Bicknell, and David H. Adams. "Hepatic sinusoidal endothelium avidly binds platelets in an integrin-dependent manner, leading to platelet and endothelial activation and leukocyte recruitment." American Journal of Physiology-Gastrointestinal and Liver Physiology 304, no. 5 (2013): G469—G478. http://dx.doi.org/10.1152/ajpgi.00407.2012.

Full text

Abstract:

Platelets have recently been shown to drive liver injury in murine models of viral hepatitis and promote liver regeneration through the release of serotonin. Despite their emerging role in inflammatory liver disease, little is known about the mechanisms by which platelets bind to the hepatic vasculature. Therefore, we referenced public expression data to determine the profile of potential adhesive receptors expressed by hepatic endothelium. We then used a combination of tissue-binding and flow-based endothelial-binding adhesion assays to show that resting platelets bind to human hepatic sinuso

APA, Harvard, Vancouver, ISO, and other styles

45

Eldor, A., I. Vlodavsky, U. Martinowicz, Z. Fuks, and BS Coller. "Platelet interaction with subendothelial extracellular matrix: platelet- fibrinogen interactions are essential for platelet aggregation but not for the matrix-induced release reaction." Blood 65, no. 6 (1985): 1477–83. http://dx.doi.org/10.1182/blood.v65.6.1477.bloodjournal6561477.

Full text

Abstract:

Abstract Cultured endothelial cells produce an extracellular matrix (ECM) to which platelets adhere and spread, ultimately resulting in platelet aggregation, thromboxane B2 production, and serotonin release. We have investigated the role of fibrinogen binding to the platelet GPIIb/IIIa complex in these reactions by comparing normal platelet-rich plasma (PRP), PRP from patients with Glanzman's thrombasthenia (whose platelets lack the GPIIb/IIIa complex), PRP in the presence of a monoclonal antibody that blocks the binding of fibrinogen to the GPIIb/IIIa complex, platelets washed free of fibrino

APA, Harvard, Vancouver, ISO, and other styles

46

Rinder, HM, JL Bonan, CS Rinder, KA Ault, and BR Smith. "Dynamics of leukocyte-platelet adhesion in whole blood." Blood 78, no. 7 (1991): 1730–37. http://dx.doi.org/10.1182/blood.v78.7.1730.1730.

Full text

Abstract:

Abstract The dynamics of leukocyte-platelet adhesion and platelet-platelet interaction in whole blood are not well understood. Using different platelet agonists, we have studied the whole blood kinetics of these heterotypic and homotypic interactions, the relative abilities of different leukocyte subsets to participate in platelet adhesion, and the ligands responsible for adhesion. When platelet aggregation was inhibited by the Arg-Gly-Asp-Ser (RGDS) peptide, thrombin stimulation of whole blood resulted in platelet expression of granule membrane protein 140 (GMP-140) and, simultaneously, a mar

APA, Harvard, Vancouver, ISO, and other styles

47

Rinder, HM, JL Bonan, CS Rinder, KA Ault, and BR Smith. "Dynamics of leukocyte-platelet adhesion in whole blood." Blood 78, no. 7 (1991): 1730–37. http://dx.doi.org/10.1182/blood.v78.7.1730.bloodjournal7871730.

Full text

Abstract:

The dynamics of leukocyte-platelet adhesion and platelet-platelet interaction in whole blood are not well understood. Using different platelet agonists, we have studied the whole blood kinetics of these heterotypic and homotypic interactions, the relative abilities of different leukocyte subsets to participate in platelet adhesion, and the ligands responsible for adhesion. When platelet aggregation was inhibited by the Arg-Gly-Asp-Ser (RGDS) peptide, thrombin stimulation of whole blood resulted in platelet expression of granule membrane protein 140 (GMP-140) and, simultaneously, a marked incre

APA, Harvard, Vancouver, ISO, and other styles

48

Lagadec, Patricia, Olivier Dejoux, Michel Ticchioni, et al. "Involvement of a CD47-dependent pathway in platelet adhesion on inflamed vascular endothelium under flow." Blood 101, no. 12 (2003): 4836–43. http://dx.doi.org/10.1182/blood-2002-11-3483.

Full text

Abstract:

AbstractResting platelet adhesion to inflammatory vascular endothelium is thought to play a causal role in secondary thrombus formation or microcirculatory disturbance after vessel occlusion. However, though adhesion receptors involved in platelet-matrix interactions have been extensively studied, the molecular mechanisms involved in platelet-endothelium interactions are incompletely characterized and have been mainly studied under static conditions. Using human platelets or platelets from wild-type and CD47–/– mice in whole blood, we demonstrated that at low shear rate, CD47 expressed on huma

APA, Harvard, Vancouver, ISO, and other styles

49

Vitkovsky, Yuri, Grigory Brill, Alexander Koltakov, et al. "Platelets enhance CD4+ lymphocyte adhesion to extracellular matrix under flow conditions: Role of platelet aggregation, integrins, and non-integrin receptors." Thrombosis and Haemostasis 95, no. 05 (2006): 815–21. http://dx.doi.org/10.1160/th05-07-0524.

Full text

Abstract:

SummaryThe purpose of this study was to examine the role of platelets in CD4+ T lymphocyte adhesion to subendothelial extracellular matrix (ECM). Herpesvirus saimiri (HVS)-infected CD4+ T cells were incubated on ECM. An image analysis was used to evaluate T cell adhesion. Under static condition, T cell activation with 4-α-Phorbol 12-myristate 13-acetate (PMA) resulted in a 2.6-fold increase in cell adhesion. However, adhesion was not affected by platelets. In contrast, under flow (200s−1), platelets markedly enhanced both resting and PMA-activatedT cell adhesion (33- and 48-fold), forming lymp

APA, Harvard, Vancouver, ISO, and other styles

50

Evangelista, V., S. Manarini, S. Rotondo, et al. "Platelet/polymorphonuclear leukocyte interaction in dynamic conditions: evidence of adhesion cascade and cross talk between P-selectin and the beta 2 integrin CD11b/CD18." Blood 88, no. 11 (1996): 4183–94. http://dx.doi.org/10.1182/blood.v88.11.4183.4183.

Full text

Abstract:

Abstract Adhesion between platelets and polymorphonuclear leukocytes (PMN) is a key event in thrombosis and inflammation. Double color fluorescence- activated cell sorter (FACS) analysis was used to determine the extent and kinetics of adhesion of thrombin-activated platelets to resting or activated PMN when mixed cell populations were incubated in dynamic conditions. Activated platelets bound very rapidly to PMN. Mixed cell conjugates reached a maximum at 1 minute and were reversible within 10 minutes. Platelet/PMN adhesion required both Ca2+ and Mg2+ and was markedly increased by the presenc

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!