scholarly journals Signaling Pathways of Receptors Involved in Platelet Activation andShedding of These Receptors in Stored Platelets

2019 ◽  
Vol 9 (1) ◽  
pp. 38-47 ◽  
Author(s):  
Asra Amelirad ◽  
Karim Shamsasenjan ◽  
Parvin Akbarzadehlaleh ◽  
Davoud Pashoutan Sarvar
Keyword(s):  
Cell Surface ◽  
Signaling Pathways ◽  
Platelet Activation ◽  
Room Temperature ◽  
Surface Receptors ◽  
Platelet Receptors ◽  
Cell Functions ◽  
Short Lifespan ◽  
Surrounding Environment

All cells encounter various signals coming from the surrounding environment and they need toreceive and respond to these signals in order to perform their functions. Cell surface receptorsare responsible for signal transduction .Platelets are blood cells which perform several functionsusing diverse receptors. Platelet concentrate is one of the most consumed blood products.However, due to the short lifespan of the platelets and platelets damage during storage, we faceshortage of platelet products. One of the damages that platelets undergo during storage is theloss of surface receptors. Since cell surface receptors are responsible for all cell functions, theloss of platelet receptors reduces the quality of platelet products. In this study, we reviewed theimportant receptors involved in platelet activation and their associated signaling pathways. Wealso looked at the platelet receptors that shed during storage and the causes of this incident.We found that GPIbα, P-selectin, CD40 and GPVI are platelet receptors that fall during plateletstorage at room temperature. Considering that GPVI and GPIbα are the most important receptorswhich involved in platelet activation, their shedding can cause decrease in platelet activationafter transfusion and decrease thrombus consistence. Shear stress and platelet contact with thecontainer wall are among the mechanisms discussed in this process, but studies in this area haveto be continued.

scholarly journals Murine Polyomavirus Cell Surface Receptors Activate Distinct Signaling Pathways Required for Infection

mBio ◽  
2016 ◽  
Vol 7 (6) ◽  
Author(s):  
Samantha D. O’Hara ◽  
Robert L. Garcea
Keyword(s):  
Cell Surface ◽  
Cell Signaling ◽  
Signaling Pathways ◽  
Mapk Pathway ◽  
Virus Entry ◽  
Pi3k Pathway ◽  
Cell Surface Receptors ◽  
Virus Binding ◽  
Surface Receptors ◽  
Host Signaling

ABSTRACTVirus binding to the cell surface triggers an array of host responses, including activation of specific signaling pathways that facilitate steps in virus entry. Using mouse polyomavirus (MuPyV), we identified host signaling pathways activated upon virus binding to mouse embryonic fibroblasts (MEFs). Pathways activated by MuPyV included the phosphatidylinositol 3-kinase (PI3K), FAK/SRC, and mitogen-activated protein kinase (MAPK) pathways. Gangliosides and α4-integrin are required receptors for MuPyV infection. MuPyV binding to both gangliosides and the α4-integrin receptors was required for activation of the PI3K pathway; however, either receptor interaction alone was sufficient for activation of the MAPK pathway. Using small-molecule inhibitors, we confirmed that the PI3K and FAK/SRC pathways were required for MuPyV infection, while the MAPK pathway was dispensable. Mechanistically, the PI3K pathway was required for MuPyV endocytosis, while the FAK/SRC pathway enabled trafficking of MuPyV along microtubules. Thus, MuPyV interactions with specific cell surface receptors facilitate activation of signaling pathways required for virus entry and trafficking. Understanding how different viruses manipulate cell signaling pathways through interactions with host receptors could lead to the identification of new therapeutic targets for viral infection.IMPORTANCEVirus binding to cell surface receptors initiates outside-in signaling that leads to virus endocytosis and subsequent virus trafficking. How different viruses manipulate cell signaling through interactions with host receptors remains unclear, and elucidation of the specific receptors and signaling pathways required for virus infection may lead to new therapeutic targets. In this study, we determined that gangliosides and α4-integrin mediate mouse polyomavirus (MuPyV) activation of host signaling pathways. Of these pathways, the PI3K and FAK/SRC pathways were required for MuPyV infection. Both the PI3K and FAK/SRC pathways have been implicated in human diseases, such as heart disease and cancer, and inhibitors directed against these pathways are currently being investigated as therapies. It is possible that these pathways play a role in human PyV infections and could be targeted to inhibit PyV infection in immunosuppressed patients.

scholarly journals Research Progress on NK Cell Receptors and Their Signaling Pathways

2020 ◽  
Vol 2020 ◽  
pp. 1-14 ◽  
Author(s):  
Yingying Chen ◽  
Dan Lu ◽  
Alexey Churov ◽  
Rong Fu
Keyword(s):  
Cell Surface ◽  
Nk Cells ◽  
Signaling Pathways ◽  
Nk Cell ◽  
Research Progress ◽  
Inhibitory Receptors ◽  
Cell Receptors ◽  
Surface Receptors ◽  
Nk Cell Receptors ◽  
Activating Receptors

Natural killer cells (NK cells) play an important role in innate immunity. NK cells recognize self and nonself depending on the balance of activating receptors and inhibitory receptors. After binding to their ligands, NK cell receptors trigger subsequent signaling conduction and then determine whether NK is activated or inhibited. Furthermore, NK cell response includes cytotoxicity and cytokine release, which is tightly related to the activation of NK cell-activating receptors and the inhibition of inhibitory receptors on the surfaces of NK cells. The expression and function of NK cell surface receptors also alter in virus infection, tumor, and autoimmune diseases and influence the occurrence and development of diseases. So, it is important to understand the mechanism of recognition between NK receptors and their ligands in pathological conditions and the signaling pathways of NK cell receptors. This review mainly summarizes the research progress on NK cell surface receptors and their signal pathways.

scholarly journals Pathogenic Hantaviruses Direct the Adherence of Quiescent Platelets to Infected Endothelial Cells

2010 ◽  
Vol 84 (9) ◽  
pp. 4832-4839 ◽  
Author(s):  
Irina N. Gavrilovskaya ◽  
Elena E. Gorbunova ◽  
Erich R. Mackow
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Surface ◽  
Vascular Permeability ◽  
Platelet Activation ◽  
Hantaan Virus ◽  
Integrin Receptors ◽  
Fab Fragment ◽  
Endothelial Cell Surface ◽  
Cell Functions

ABSTRACT Hantavirus infections are noted for their ability to infect endothelial cells, cause acute thrombocytopenia, and trigger 2 vascular-permeability-based diseases. However, hantavirus infections are not lytic, and the mechanisms by which hantaviruses cause capillary permeability and thrombocytopenia are only partially understood. The role of β3 integrins in hemostasis and the inactivation of β3 integrin receptors by pathogenic hantaviruses suggest the involvement of hantaviruses in altered platelet and endothelial cell functions that regulate permeability. Here, we determined that pathogenic hantaviruses bind to quiescent platelets via a β3 integrin-dependent mechanism. This suggests that platelets may contribute to hantavirus dissemination within infected patients and provides a means by which hantavirus binding to β3 integrin receptors prevents platelet activation. The ability of hantaviruses to bind platelets further suggested that cell-associated hantaviruses might recruit platelets to the endothelial cell surface. Our findings indicate that Andes virus (ANDV)- or Hantaan virus (HTNV)-infected endothelial cells specifically direct the adherence of calcein-labeled platelets. In contrast, cells comparably infected with nonpathogenic Tula virus (TULV) failed to recruit platelets to the endothelial cell surface. Platelet adherence was dependent on endothelial cell β3 integrins and neutralized by the addition of the anti-β3 Fab fragment, c7E3, or specific ANDV- or HTNV-neutralizing antibodies. These findings indicate that pathogenic hantaviruses displayed on the surface of infected endothelial cells bind platelets and that a platelet layer covers the surface of infected endothelial cells. This fundamentally changes the appearance of endothelial cells and has the potential to alter cellular immune responses, platelet activation, and endothelial cell functions that affect vascular permeability. Hantavirus-directed platelet quiescence and recruitment to vast endothelial cell beds further suggests mechanisms by which hantaviruses may cause thrombocytopenia and induce hypoxia. These findings are fundamental to our understanding of pathogenic-hantavirus regulation of endothelial cell responses that contribute to vascular permeability.

scholarly journals Phagocytic Receptors Activate Syk and Src Signaling during Borrelia burgdorferi Phagocytosis

2017 ◽  
Vol 85 (10) ◽  
Author(s):  
Tess L. Killpack ◽  
Maria Ballesteros ◽  
Stephen C. Bunnell ◽  
Alice Bedugnis ◽  
Lester Kobzik ◽  
...  
Keyword(s):  
Lyme Disease ◽  
Cell Surface ◽  
Borrelia Burgdorferi ◽  
Signaling Pathways ◽  
Cell Surface Receptors ◽  
Integrin Β1 ◽  
Content Type ◽  
Surface Receptors ◽  
Src Signaling ◽  
Cytokine Activation

ABSTRACT Phagocytosis of the Lyme disease-causing pathogen Borrelia burgdorferi has been shown to be important for generating an inflammatory response to the pathogen. As a result, understanding the mechanisms of phagocytosis has been an area of great interest in the field of Lyme disease. Several cell surface receptors that participate in B. burgdorferi phagocytosis have been reported, including the scavenger receptor MARCO and integrin α3β1. We sought to define the mechanisms by which these receptors mediate phagocytosis and to identify signaling pathways activated downstream of these receptors upon contact with B. burgdorferi. We identified both Syk and Src signaling pathways as ones that participate in B. burgdorferi phagocytosis and the resulting cytokine activation. In our studies, we found that both MARCO and integrin β1 play a role in the activation of the Src kinase pathway. However, only integrin β1 participates in the activation of Syk. Interestingly, the integrin activates Syk without the help of the signaling adaptor Dap12 or FcRγ. Thus, we report that multiple pathways participate in B. burgdorferi internalization and that different cell surface receptors act simultaneously in cooperation and independently to mediate phagocytosis.

scholarly journals Molecular Drivers of Platelet Activation: Unraveling Novel Targets for Anti-Thrombotic and Anti-Thrombo-Inflammatory Therapy

2020 ◽  
Vol 21 (21) ◽  
pp. 7906
Author(s):  
Madhumita Chatterjee ◽  
Agnes Ehrenberg ◽  
Laura Mara Toska ◽  
Lisa Maria Metz ◽  
Meike Klier ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Platelet Activation ◽  
Chemokine Receptors ◽  
Thrombus Formation ◽  
Shape Change ◽  
Inflammatory Cells ◽  
Organ Damage ◽  
The Past ◽  
Platelet Shape

Cardiovascular diseases (CVDs) are the leading cause of death globally—partly a consequence of increased population size and ageing—and are major contributors to reduced quality of life. Platelets play a major role in hemostasis and thrombosis. While platelet activation and aggregation are essential for hemostasis at sites of vascular injury, uncontrolled platelet activation leads to pathological thrombus formation and provokes thrombosis leading to myocardial infarction or stroke. Platelet activation and thrombus formation is a multistage process with different signaling pathways involved to trigger platelet shape change, integrin activation, stable platelet adhesion, aggregation, and degranulation. Apart from thrombotic events, thrombo-inflammation contributes to organ damage and dysfunction in CVDs and is mediated by platelets and inflammatory cells. Therefore, in the past, many efforts have been made to investigate specific signaling pathways in platelets to identify innovative and promising approaches for novel antithrombotic and anti-thrombo-inflammatory strategies that do not interfere with hemostasis. In this review, we focus on some of the most recent data reported on different platelet receptors, including GPIb-vWF interactions, GPVI activation, platelet chemokine receptors, regulation of integrin signaling, and channel homeostasis of NMDAR and PANX1.

Defibrotide Inhibits Platelet Activation by Cathepsin G Released From Stimulated Polymorphonuclear Leukocytes

1992 ◽  
Vol 67 (06) ◽  
pp. 660-664 ◽  
Author(s):  
Virgilio Evangelista ◽  
Paola Piccardoni ◽  
Giovanni de Gaetano ◽  
Chiara Cerletti
Keyword(s):  
Platelet Activation ◽  
Polymorphonuclear Leukocytes ◽  
Direct Interaction ◽  
Cathepsin G ◽  
In Vivo Test ◽  
Cell Functions ◽  
Test Models ◽  
Antithrombotic Effects

SummaryDefibrotide is a polydeoxyribonucleotide with antithrombotic effects in experimental animal models. Most of the actions of this drug have been observed in in vivo test models but no effects have been reported in in vitro systems. In this paper we demonstrate that defibrotide interferes with polymorphonuclear leukocyte-induced human platelet activation in vitro. This effect was not related to any direct interaction with polymorphonuclear leukocytes or platelets, but was due to the inhibition of cathepsin G, the main biochemical mediator of this cell-cell cooperation. Since cathepsin G not only induces platelet activation but also affects some endothelial cell functions, the anticathepsin G activity of defibrotide could help to explain the antithrombotic effect of this drug.

THE STUDY ON TA VAT WINE PRODUCTION FROM SUGAR PALM (ARENGA PINNATA) SAP

2014 ◽  
Vol 83 (5) ◽  
Author(s):  
Nguyễn Thị Hồng Thu ◽  
Đặng Minh Nhật ◽  
Nguyễn Hoàng Dung
Keyword(s):  
Room Temperature ◽  
Fermentation Process ◽  
Inoculum Size ◽  
Wine Fermentation ◽  
Wine Production ◽  
Factors Affecting ◽  
Natural Fermentation ◽  
Tropical Asia ◽  
Best Parameters

Sugar palm (Arenga pinnata) is a feather palm native to tropical Asia. In Vietnam, it is named Búng Báng or Đoác and grown only on the highlands in the central or northern part of Vietnam. It is utilized for many purposes, especially for Ta Vat wine production - a characteristic and unique product of Co Tu ethnic minority. However, because of the natural fermentation used in the production, the product quality is inconsistent. The purpose of this study was to examine a new procedure of using palm sap for making Ta Vat wine. Some characteristics of the sap, which was collected at Nam Giang district, Quang Nam province are determined, proving the potential of the sap for making wine product. The quality of sap changes quickly at room temperature. At low temperature (4 - 60C), the changes in sap quality are apparently slower. Examining some factors affecting its quality during the wine fermentation process, we determined the best parameters for the fermentation process as follows: inoculum size of 3% with cell density of about 1x108 cells/ml, the addition of the extract from the bark of Ceylon ironwood (Mesua ferrea L.) 4%. Keywords: Arenga pinnata, sap, Ceylon ironwood bark, Mesua ferrea L., wine fermentation.

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