scholarly journals Broad-Spectrum Anti-Adhesive Coating Based on an Extracellular Polymer from a Marine Cyanobacterium

Marine Drugs ◽  
2019 ◽  
Vol 17 (4) ◽  
pp. 243 ◽  
Author(s):  
Bruna Costa ◽  
Rita Mota ◽  
Paula Parreira ◽  
Paula Tamagnini ◽  
M. Cristina L. Martins ◽  
...  
Keyword(s):  
Medical Device ◽  
Plasma Proteins ◽  
Bacterial Resistance ◽  
Thrombus Formation ◽  
Adhesive Properties ◽  
Marine Cyanobacterium ◽  
Technological Platform ◽  
Etiological Agents ◽  
Extracellular Polymer ◽  
Adhesive Coating

Medical device-associated infections are a major health threat, representing about half of all hospital-acquired infections. Current strategies to prevent this problem based on device coatings with antimicrobial compounds (antibiotics or antiseptics) have proven to be insufficient, often toxic, and even promoting bacterial resistance. Herein, we report the development of an infection-preventive coating (CyanoCoating) produced with an extracellular polymer released by the marine cyanobacterium Cyanothece sp. CCY 0110. CyanoCoating was prepared by spin-coating and its bacterial anti-adhesive efficiency was evaluated against relevant etiological agents (Staphylococcus aureus, S. epidermidis, Pseudomonas aeruginosa and Escherichia coli) and platelets, both in the presence or absence of human plasma proteins. CyanoCoating cytotoxicity was assessed using the L929 fibroblasts cell line. CyanoCoating exhibited a smooth topography, low thickness and high hydrophilic properties with mild negative charge. The non-cytotoxic CyanoCoating prevented adhesion of all the bacteria tested (≤80%) and platelets (<87%), without inducing platelet activation (even in the presence of plasma proteins). The significant reduction in protein adsorption (<77%) confirmed its anti-adhesive properties. The development of this anti-adhesive coating is an important step towards the establishment of a new technological platform capable of preventing medical device-associated infections, without inducing thrombus formation in blood-contacting applications.

scholarly journals The Small GTPase Rap1b: A Bidirectional Regulator of Platelet Adhesion Receptors

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Gianni Francesco Guidetti ◽  
Mauro Torti
Keyword(s):  
Cell Adhesion ◽  
Signaling Pathways ◽  
Platelet Adhesion ◽  
Thrombus Formation ◽  
Small Gtpases ◽  
Small Gtpase ◽  
Complex Pattern ◽  
Adhesive Properties ◽  
Adhesion Receptors ◽  
Inside Out

Integrins and other families of cell adhesion receptors are responsible for platelet adhesion and aggregation, which are essential steps for physiological haemostasis, as well as for the development of thrombosis. The modulation of platelet adhesive properties is the result of a complex pattern of inside-out and outside-in signaling pathways, in which the members of the Rap family of small GTPases are bidirectionally involved. This paper focuses on the regulation of the main Rap GTPase expressed in circulating platelets, Rap1b, downstream of adhesion receptors, and summarizes the most recent achievements in the investigation of the function of this protein as regulator of platelet adhesion and thrombus formation.

2008 Sol Sherry Distinguished Lecture in Thrombosis—Platelet Adhesion in Acute Arterial Thrombosis

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Zaverio M. Ruggeri
Keyword(s):  
Vascular Injury ◽  
Blood Cells ◽  
Platelet Adhesion ◽  
Cancer Metastasis ◽  
Thrombus Formation ◽  
Arterial Occlusion ◽  
Vascular Wall ◽  
Membrane Receptors ◽  
Adhesive Properties ◽  
Vascular Integrity

Platelet adhesion is an essential function in response to vascular injury, through which single platelets bind to specific membrane receptors onto cellular and extracellular matrix constituents of the vessel wall and tissues initiating thrombus formation that arrests hemorrhage and permits wound healing. Pathological conditions that cause vascular alterations and blood flow disturbances may turn this defense process into a disease mechanism resulting in arterial occlusion, mostly in atherosclerotic vessels of the heart and brain. Besides their relevant role in hemostasis and thrombosis, platelet adhesive properties are central to a variety of pathophysiological processes that extend from inflammation to immune-mediated host defense and pathogenic mechanisms as well as cancer metastasis. All these activities depend on the ability of platelets to circulate in blood as sentinels of vascular integrity, adhere where alterations are detected, and signal the abnormality to other platelets and blood cells. In this respect, therefore, platelet adhesion to vascular wall structures, to one another (aggregation), or to other blood cells represents different aspects of the same fundamental biological process. Novel concepts and tools are being developed to advance our knowledge of the mechanisms through which platelets respond to vascular injury. Of particular interest are specific microparticles endowed with selective targeting properties conferred by recombinant adhesive domains that may be used for targeting areas of the vasculature with thrombogenic potential and for diagnostic purposes. Particles with such specific adhesive properties may also be used for the local delivery of anti-thrombotic drugs.

Role of Integrin αvβ3 in Vascular Biology

1998 ◽  
Vol 80 (11) ◽  
pp. 726-734 ◽  
Author(s):  
Tatiana Byzova ◽  
Ramin Rabbani ◽  
Stanley D’Souza ◽  
Edward Plow
Keyword(s):  
Cell Biology ◽  
Cell Function ◽  
Thrombus Formation ◽  
Cellular Adhesion ◽  
Vascular Cells ◽  
Functional Responses ◽  
Adhesive Properties ◽  
Adhesion Receptors ◽  
Vascular Cell

IntroductionA defining characteristic of vascular cells is their adhesive status. The predominant cells of the blood vessel, endothelial cells (EC) and smooth muscle cells (SMC), are normally adherent but can be induced to migrate in response to vascular injury and angiogenic stimuli. The circulating blood cells are ordinarily nonadhesive but can rapidly acquire an adhesive phenotype in response to physiologic and pathophysiologic stimuli. As prime examples, platelets become adherent to the subendothelial matrix and to one another during thrombus formation, and leukocytes first adhere to EC and then transmigrate during the inflammatory response. At a molecular level, the adhesive properties of the vascular cells are determined by the adhesion receptors on their cell-surface and the functional state of these receptors. To match the variety of requisite cellular adhesive reactions, the repertoire of adhesion receptors expressed by vascular cells is broad. Multiple representatives of the immunoglobulin-like, the selectin, the cadherin and the integrin families of adhesion receptors are present on and have been implicated in the functions of the vascular cells. The importance of these adhesion receptors in vascular cell function is underscored by the severe pathogenetic consequences of their congenital deficiencies, such as in Glanzmann’s thrombasthenia, LAD (Leucocyte Adhesion deficiency) I and LAD II (1-3).The integrins are the largest and most broadly distributed of the families of cellular adhesion receptors. Of the integrins, αvβ3, originally identified as the vitronectin receptor, is particularly widely distributed. It is expressed at variable density on many types of vascular cells. Obviously, the adhesive properties of a cell are determined by its full repertoire of adhesion receptors. As an example, the adhesion of EC to fibrinogen/fibrin is mediated by no fewer than five receptors. Nevertheless, it is possible to dissect out the contributions of individual adhesion receptors, and αvβ3 has been implicated in many functional responses of vascular cells. This review focusses upon the role of αvβ3 in vascular cell biology. Other contributions of this multifunctional receptor, such as its role in neoplastic growth and invasion and in osteoclast-mediated bone resorption, are beyond the scope of this article and have been reviewed elsewhere (4, 5).

The Dura as Anti-Adhesive Coating Polypropylene Implant for Laparoscopic Hernioplasty

10.12737/5948 ◽  
2014 ◽  
Vol 8 (1) ◽  
pp. 1-5
Author(s):  
Воробейчук ◽  
G. Vorobeychuk ◽  
Драйер ◽  
M. Drayer ◽  
Тлибекова ◽  
...  
Keyword(s):  
Connective Tissue ◽  
Wistar Rats ◽  
Research Work ◽  
Parietal Peritoneum ◽  
Grid Structure ◽  
Adhesive Properties ◽  
Internal Organs ◽  
Laparoscopic Hernioplasty ◽  
Adhesive Coating

This study presents the results of investigation of anti-adhesive properties of the dura combined with polypropylene implant, and a composite mash with a hydrogellayer Parietex Composite. 40 Wistar rats were used for this research work. The study showed that the use of the dura as an anti-adhesive coating prevents fusion of the internal organs with the implant, and the polypropylene used as a mash basis, firmly fuses with the parietal peritoneum, promoting in growth of connective tissue in the grid structure. These results are comparable to results obtained using Parietex Composite.

Extracellular RNA

2007 ◽  
Vol 27 (05) ◽  
pp. 373-377 ◽  
Author(s):  
K. T. Preissner
Keyword(s):  
Blood Coagulation ◽  
Plasma Proteins ◽  
Defense Mechanisms ◽  
Thrombus Formation ◽  
Danger Signal ◽  
Edema Formation ◽  
Extracellular Rna ◽  
Life Threatening

SummaryUpon vascular injury, locally controlled haemostasis prevents life threatening blood loss and ensures wound healing. Intracellular material derived from damaged cells at these sites will become exposed to cells and plasma proteins and could thereby influence vascular homeostasis, blood coagulation and defense mechanisms. Recently, this concept was documented by several studies indicating that extracellular nucleic acids, and RNA in particular, serve as promoter of blood coagulation in vivo and significantly increase the permeability across brain endothelial cells in vitro and in vivo. As procoagulant cofactor and ,,natural foreign material“, RNA triggers the contactphase pathway of blood coagulation and thereby contributes to pathological thrombus formation. Administration of RNase significantly delayed occlusive thrombus formation and prevented edema formation in different animal models. Thus, extracellular RNA derived from damaged and necrotic cells may serve as a natural danger signal that contributes to initiation of host defense mechanisms, while antagonizing RNase provides new regimens for antithrombotic and vessel-protective therapies.

scholarly journals Natural Cyanobacterial Polymer-Based Coating as a Preventive Strategy to Avoid Catheter-Associated Urinary Tract Infections

Marine Drugs ◽  
2020 ◽  
Vol 18 (6) ◽  
pp. 279 ◽  
Author(s):  
Bruna Costa ◽  
Rita Mota ◽  
Paula Tamagnini ◽  
M. Cristina L. Martins ◽  
Fabíola Costa
Keyword(s):  
Urinary Tract ◽  
Urinary Tract Infections ◽  
Preventive Strategy ◽  
E Coli ◽  
Artificial Urine ◽  
Etiological Agents ◽  
Tract Infections ◽  
Healthcare Associated ◽  
Further Development ◽  
Adhesive Coating

Catheter-associated urinary tract infections (CAUTIs) represent about 40% of all healthcare-associated infections. Herein, the authors report the further development of an infection preventive anti-adhesive coating (CyanoCoating) meant for urinary catheters, and based on a natural polymer released by a marine cyanobacterium. CyanoCoating performance was assessed against relevant CAUTI etiological agents, namely Escherichia coli, Proteus mirabilis, Klebsiella pneumoniae, methicillin resistant Staphylococcus aureus (MRSA), and Candida albicans in the presence of culture medium or artificial urine, and under biofilm promoting settings. CyanoCoating displayed a broad anti-adhesive efficiency against all the uropathogens tested (68–95%), even in the presence of artificial urine (58–100%) with exception of P. mirabilis in the latter condition. Under biofilm-promoting settings, CyanoCoating reduced biofilm formation by E. coli, P. mirabilis, and C. albicans (30–60%). In addition, CyanoCoating prevented large crystals encrustation, and its sterilization with ethylene oxide did not impact the coating stability. Therefore, CyanoCoating constitutes a step forward for the implementation of antibiotic-free alternative strategies to fight CAUTIs.

Development of a Stable Thrombotic Core with Limited Access to Plasma Proteins During Thrombus Formation In Vivo

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2013-2013 ◽  
Author(s):  
Timothy J. Stalker ◽  
Elizabeth A. Traxler ◽  
Scott L. Diamond ◽  
Lawrence F. Brass
Keyword(s):  
Vascular Injury ◽  
Central Region ◽  
Plasma Proteins ◽  
Conflicts Of Interest ◽  
Thrombus Formation ◽  
Surface Expression ◽  
Activation Markers ◽  
Platelet Surface ◽  
Platelet Accumulation

Abstract Abstract 2013 Several studies examining thrombus formation in vivo have described the formation of a thrombotic core composed of stably adherent, apparently activated platelets covered by several layers of minimally activated, loosely adherent platelets. Using confocal fluorescence intravital microscopy in mouse cremaster muscle arterioles, we sought to 1) determine whether the stable thrombus core could be defined by the presence of platelet activation markers (e.g. P-selectin); 2) define the spatial and temporal characteristics of the stable thrombus core as it develops; and 3) determine whether the accessibility of plasma proteins to the inner regions of a stable thrombus is limited. We found that P-selectin platelet surface expression is associated with stable platelet incorporation into a growing thrombus following either laser- or wall puncture-induced vascular injury in vivo. The P-selectin positive core originated at the site of vascular injury and subsequently expanded outward into the central region of the developing thrombus with kinetics that were distinct from total platelet accumulation. Further, using two related approaches, we determined that the accessibility of plasma components to the stable thrombus core is limited. In the first approach, fluorescently labeled anti-P-selectin antibody was infused after a stable thrombus had formed (25 minutes after injury), and was found to bind to a monolayer of platelets on the luminal surface of the stable thrombus core, but was unable to penetrate this layer of platelets and bind to platelets in the central region of the thrombus. In the second approach, we directly measured the porosity of thrombi as they evolved by infusing fluorescently labeled dextran to illuminate the plasma in the gaps between platelets. We found that the porosity of the stable thrombus core was significantly decreased as compared to the porosity of the growing platelet mass before the core developed. Taken together, these results demonstrate that a stable core composed of degranulated platelets develops during thrombus formation in vivo with spatial localization and kinetics that are distinct from total platelet accumulation, and that development of this core limits the accessibility of plasma components to the central region of a stable thrombus. Disclosures: No relevant conflicts of interest to declare.

A Flow Cytometry Method for Characterizing Platelet Activation

2020 ◽  
Author(s):  
Brian Alzua ◽  
Mark Smith ◽  
Yan Chen
Keyword(s):  
Flow Cytometry ◽  
Medical Device ◽  
Platelet Activation ◽  
Medical Devices ◽  
Whole Blood ◽  
Platelet Rich Plasma ◽  
Thrombus Formation ◽  
Standard Regimen ◽  
Activated Platelets ◽  
Wide Range

Abstract Hemocompatibility testing is critical for assessing the safety of blood-contacting medical devices. Comprehensive hemocompatibility testing requires examining a wide range of possible adverse effects cause by direct or indirect blood contact, such as hemolysis, complement activation, and thrombus formation [1]. Moreover, these domains each encompass complex intercellular processes with many potential targets for analysis. For example, the current testing paradigm of platelet function may involve exposing the device to human whole blood and performing simple blood counts and/or macroscopic evaluation to determine the extent of platelet activation and clot formation as described in ASTM F2888-19. However, this approach does not capture any observations for device-mediated initiation of any steps in the platelet activation pathway prior to aggregation. We have validated a method to evaluate platelet activation by quantifying surface p-selectin expression after exposure to various materials. This method will provide an additional level of detail about potential platelet activating properties of a medical device. Flow cytometry has been used previously to measure platelet activation for clinical and research purposes. We sought to adapt this method to test for platelet activation induced by exposure of blood to medical devices or materials. We determined that processing fresh whole blood to platelet-rich plasma (PRP) by gentle centrifugation enhanced the signal compared to fresh blood itself. In each experiment, devices were exposed to PRP according to an extraction ratio of 6 cm2/mL for 1 hour. A blank control consisting of untreated PRP, and a positive control consisting of ADP, a potent agonist, were also used. After the exposure, excess plasma was removed from the articles and combined with anti-CD61 (to stain for platelets) and anti-CD62P (to stain for activated platelets) antibodies. Flow cytometry was then performed to quantify the percentage of CD62P+ over the total CD61+ cells to measure the percentage of activated platelets. In order to optimize the method, we investigated the effect of several experimental factors, including anticoagulant usage, donor variability, and selection of reference materials to serve as controls. Our results indicate that the flow cytometry-based method is consistent and reproducible, quick and easy to perform, and is well-correlated with results from the standard platelet and leukocyte count assay. The flow cytometry-based platelet activation method is a powerful supplement to the standard regimen of medical device hemocompatibility testing.

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